The first thing to note is that changes in blood pressure constantly
occur as a response to changes in our environment and/or in our
activity. This is a normal compensating response of the body, to keep
things functioning properly. The problems start when a continually
high blood pressure is maintained, since this will eventually result
in damage to the blood vessels and heart.
A number of different mechanisms can be responsible for raising blood
pressure and these will be affected to various degrees by the
different causative agents.
There is a very detailed and technical article on this subject at
http://www.medscape.com/viewarticle/438087_1 (you need to register
with the site to view the article, but this is free of charge)
Therapeutic Considerations in the Treatment of Obesity Hypertension
by Marion R. Wofford, MD, MPH; Margaret Miller Davis, MD; Kimberly G.
Harkins, MD; Deborah S. King, PharmD; Sharon B. Wyatt, PhD, RN, CS;
Daniel W. Jones, MD
published in Journal of Clinical Hypertension 2002, Volume 4(part 3)
One section of this article is titled Mechanisms of Obesity-Induced
Hypertension. Here I will summarize, translate and explain some of
the information that is provided.
The authors say that many different mechanisms can be involved and the
many interrelations between them means it is difficult to separate
them out. They list the following:
1. Alterations in haemodynamics: a comparison of obese people with
those of normal weight shows that changes occur in the blood flow to
the kidneys, heart, muscles and intestines. The result of these
changes is to cause the heart to pump out more blood faster, thus
raising the pressure within the blood vessels. Why the changes occur
in the first place has still to be explained.
2. Insulin metabolism. This is known to change in obesity, so that
the person becomes less able to use the insulin in order to metabolise
glucose (this phenomenon is called insulin resistance) and may
eventually develop type II diabetes. Because the insulin cannot be
used so efficiently, its levels in the blood become abnormally high, a
state called hyperinsulinemia. It has been suggested that
hyperinsulinemia can cause blood pressure to increase by directly
influencing sodium excretion, causing a greater amount of sodium to be
reabsorbed from urine in the kidneys back into the body. It is also
thought to increase the activity of the sympathetic nervous system,
and to increase the response to angiotensin II in the secretion of
aldosterone. These events will cause blood pressure to increase
(further explanation will follow below). However, please note that the
authors conclude this part of the discussion with the statement: An
association between obesity and disturbance of insulin metabolism is
well established, but the relationship between
hyperinsulinemia/insulin resistance and its long-term effect on blood
pressure is unclear and currently debated.
3. Activation of the renin-angiotensin system. Obese people have
been found to have high levels of renin. Increased activity of the
sympathetic nervous system will activate this system. It is also
suggested that changes in the structure of the kidneys that occur in
obesity can affect the renin-angiotensin balance. The net result is
the increased reabsorption of sodium from urine in the kidneys back
into the body.
4. Increased activity of the sympathetic nervous system is readily
shown to be present in obesity. For example, the authors mention a
study that showed plasma norepinephrine levels (a measure of this
activity) increase with increased intake of calories and another that
found increased muscle sympathetic nerve activity in obese people.
They think this phenomenon might be associated with the activity of
leptin, a substance secreted by fat cells and linked with obesity. As
mentioned before, increased sympathetic activity stimulates the
Since being overweight makes a person more likely to have blood
pressure, a diet that is too rich in calories will be a causative
factor just for that reason.
However, there are also other ways in which diet can affect blood
pressure. For example, a high-fat diet is more likely to lead to the
deposition of fat in the arteries, causing them to narrow and lose
their elasticity (atherosclerosis). This increases the resistance of
the vessels against blood flow, which results in the development of
high pressure. At this point, a vicious circle kicks in because it is
thought that high blood pressure facilitates the development of
atherosclerosis. Some scientists have suggested that the same
mechanism is responsible for both:
The researchers said the protein Angiotensin II, which causes a
narrowing of small blood vessels and raises blood pressure, may also
promote the buildup of fatty deposits in the arteries of people with
Story on Science Daily, November 15, 1999
Substances in certain foods may have a specific effects on blood
pressure, either raising or lowering it. Again, the story can be
complex, as in this excerpt from a journal article abstract:
Dietary factors such as sodium, potassium, calcium, magnesium, zinc,
selenium, vitamins A, C, and E, and essential fatty acids and their
products such as eicosanoids can influence blood pressure
might be a close interaction between these dietary factors,
sympathetic and parasympathetic nervous systems, the metabolism of
essential fatty acids, nitric oxide, prostacyclin, and endothelium in
human essential hypertension. A deficiency in any one factor, dietary
or endogenous, or alterations in their interactions with each other,
can lead to endothelial [endothelium = tissue lining the inner surface
of blood vessel] dysfunction and development of hypertension.
Nutritional factors in the pathobiology of human essential
hypertension. by U N Das. Published in Nutrition. 2001 Apr; Vol
17(4), pages 337-346.
Licorice is known to raise blood pressure. Here is part of an
explanation from MadSci Network:
Having licorice once in a while is not damaging, but over time,
licorice ingestion can induce pseudoaldosteronism. Aldosterone is the
adrenal hormone that acts on the kidney, telling it to retain water
Licorice contains glycyrrhizin, which is absorbed as glycyrrhetinic
acid. Glycyrrhizin, inhibits an enzyme called 11-beta-hydroxysteroid
dehydrogenase, which converts cortisol to cortisone. Cortisol, but not
cortisone, binds to the aldosterone receptor in the kidney and mimicks
the effects of aldosterone, which could explain the effects of
licorice - a buildup of cortisol, which is recognized by the body as
What does pseudoaldosteronism do? Kidney retention of water and
sodium lead to increased blood volume. Increased blood volume leads to
increased blood pressure (think of it as turning up the tap on a water
hose - the more water, the more pressure on the hose).
For the whole story, go to:
Caffeine acts directly on blood vessels and makes them narrower. This
increases the resistance of the vessels to the flow of blood and so
raises blood pressure. The effects of caffeine appear to be greater
in people who are otherwise at risk for hypertension:
Studies in our laboratory and others have reported that caffeine
acutely elevates SBP and diastolic blood pressure (DBP) at rest and
during mental and exercise stress. We have shown that this pressor
effect is due to the elevation by caffeine of peripheral vascular
resistance rather than enhancement of cardiac output.
The present study demonstrates that caffeine affects persons to a
progressively greater degree according to their BP classification. It
further demonstrates that the higher the risk classification, the more
likely are BPs in the hypertensive range 45 to 60 minutes after
consumption of a dietary dose of caffeine and while resting.
Hypertension Risk Status and Effect of Caffeine on Blood Pressure
By Terry R. Hartley; Bong Hee Sung; Gwendolyn A. Pincomb; Thomas L.
Whitsett; Michael F. Wilson; William R. Lovallo
Published in Hypertension. 2000; Vol 36: p. 137-
The whole article is available at:
This is also a complex situation. The effects of alcohol will depend
on how much is taken.
Heavy drinking is associated with hypertension. A study has shown
that alcohol stimulates the activity of the sympathetic nervous
system, which as already mentioned above results in increased blood
To determine whether alcohol evokes sympathetic activation
we measured blood pressure, heart rate, and sympathetic-nerve action
in nine normal subjects before and during an intravenous infusion of
alcohol (0.5 g per kilogram of body weight over a period of 45
minutes) and for 75 minutes after the infusion.
The infusion of alcohol alone evoked a marked (P<0.001) and
progressive increase in the mean rate of sympathetic discharge,
.. This sympathetic activation was accompanied during the second
hour by an increase in mean arterial pressure of 10+/-5 mm Hg
Suppression of Alcohol-Induced Hypertension by Dexamethasone by
Denis Randin, M.D., Peter Vollenweider, M.D., Luc Tappy, M.D., Eric
Jéquier, M.D., Pascal Nicod, M.D., and Urs Scherrer, M.D.
New England Journal of Medicine, Volume 332: pages 1733-1738 June
The URL is to the summary, but you can register for free with the site
to gain access to the full text of research articles published more
than 6 months ago.
On the other hand:
Moderate alcohol consumption can lead to a reduced risk of developing
hypertension in young women, according to researchers from the
Massachusetts General Hospital (MGH) and Brigham and Women's Hospital
. the scientists found that women who drank about two or three drinks
a week had a risk of developing hypertension about 15 percent lower
than that of nondrinkers. However, women who drank on average more
than 10 or 12 drinks per week had a 30 percent increased risk of
developing the condition.
At the higher levels of consumption, all beverages - beer, wine, and
liquor - increased blood pressure, whereas there was a suggestion that
moderate beer drinking led to lower blood pressures.
Science Daily news article, 11 March, 2002
The immediate effects of smoking are an increase in heart rate, blood
pressure and respiration, and a decrease in skin temperature due to a
constriction or closing of peripheral blood vessels. Nicotine and
carbon monoxide are primarily responsible for these effects through
the stimulation of a rapid release of adrenaline, the "fight or
Medical Consequences of Smoking Liberty Science Center
Nicotine has another compounding effects. It increases cardiac output,
by causing the heart to beat faster. As a result, a greater volume of
blood is pumped around the body in a shorter time, which increases the
pressure within the blood vessels.
The smoking of one cigarette with a high content of nicotine produced
a peak rise in cardiac output of 32 percent above baseline values, and
the effect persisted for one hour. Smoking a cigarette with a low
content of nicotine produced a peak rise of 13 percent above baseline
values, with a duration of five minutes. The rise in cardiac output
was almost entirely attributable to tachycardia, since stroke volume
remained relatively constant. The smoking of a cigarette with high
nicotine content also caused greater and more sustained elevation in
systemic blood pressure than smoking a cigarette with low nicotine
Hemodynamic effects of smoking cigarettes of high and low nicotine
content By L Tachmes, RJ Fernandez and MA Sackner
Chest, 1978, Vol 74, pages 243-246
Smoking can also have an indirect effect:
Researchers at the U.S. Department of Energy's Brookhaven National
Laboratory, who previously found reduced levels of the enzyme
monoamine oxidase B (MAO B) in the brains of smokers, now provide
compelling evidence that MAO in peripheral organs -- the kidneys,
heart, lungs, and spleen -- is also affected by smoking.
The scientists administered MAO B-specific binding radiotracers
labeled with carbon -11 to twelve smokers and performed whole-body PET
scans to measure the level of MAO B in various organs. They then
compared the results with those from a group of eight nonsmokers.
One of the functions performed by MAO in the body is to break down
chemical compounds that elevate blood pressure, such as chemicals
found in certain foods like cheese and wine, as well as some chemicals
that are released by nicotine. Thus, the health consequences of
reduced MAO B may be indirect and associated with other dietary
substances or environmental compounds normally broken down by the
EurekAlert news article, 8 Sept, 2003
Vigorous exercise does indeed increase blood pressure while it is
going on. This is a normal response of the body. During exercise,
blood flow to muscles increases, so that the muscles can be supplied
with enough oxygen for the work that they are doing.
Peripheral resistance decreases during exercise. This occurs because
of the tremendous increase in blood flow to working skeletal muscle.
Vasoconstriction in nonexercising tissue is not enough to compensate
for the vasodilation in active muscles. Blood pressure does not fall
during exercise, it increases. Cardiac output increases greatly during
exercise, which more than compensates for the fall in peripheral
resistance. For example, in a fit 20 yr old male, cardiac output will
increase from about 5 liters at rest to approximately 20 liters during
maximal exercise. Even though peripheral resistance may fall by almost
300 percent during exercise, systolic blood pressure increases.
Blood Pressure Response During Exercise by Thomas D. Fahey
However, although blood pressure increases during exercise, the
overall effect of exercise is to decrease the chance of developing
Sedentary individuals with normal blood pressure have an increased
risk of developing hypertension when compared with more active and fit
peers. In studies looking at the effects of aerobic exercise training
in hypertensive patients, average blood pressure reduction ranges from
4 mm Hg-10 mm Hg.
From Therapeutic Considerations in the Treatment of Obesity
Hypertension by Marion R. Wofford (the first article listed in this
You will have noticed in what has been said above, that the end result
of some of the mechanisms involved is to cause more sodium to be
reabsorbed from the urine, thus increasing levels of sodium in the
body. A high intake of sodium in the diet will also increase sodium
levels in the body and increase blood pressure, although the size of
the effect varies between individuals:
The National Heart, Lung, and Blood Institute (NHLBI) organized a
workshop on this topic in 1999. You can read a summary at:
The NHLBI Workshop on Sodium and Blood Pressure: A Critical Review of
Current Scientific Evidence by Aram V. Chobanian, M.D., Workshop
Co-Chair Professor, Department of Medicine
Dean, Boston University School of Medicine Boston, Massachusetts
Martha Hill, R.N. Ph.D., Workshop Co-Chair Professor Johns Hopkins
University School of Nursing
There is quite a lot of discussion about the effects of diet in
general on blood pressure, although mechanisms are not discussed.
With respect to sodium, the following points are made in the summary:
An abundance of scientific evidence indicates that higher sodium
consumption is associated with higher levels of blood pressure. This
evidence is found in animal studies, observational epidemiologic
studies, and clinical studies and trials. The summary describes some
of this evidence.
The size of the effect that sodium has on blood pressure varies
between individuals. The workshop participants concluded:
In addition to age, race, and genetic background, response to sodium
also may be influenced by medications, the intake of other nutrients,
and the duration of the exposure.
The sodium in the body is mainly found in the extracellular fluid
(ECF) and plasma. The actual concentration of sodium is controlled
very strictly by a number of mechanisms, of which vasopressin is one
of the most important. Vasopressin regulates how much water is
retained in the body or excreted by the kidneys.
A chronic increase in the total quantity of sodium chloride in the
body leads to a chronic increase in ECF volume, part of which is
proportionately distributed to the blood volume compartment.
. Chronic increases in blood volume increase mean circulatory
pressure and lead
to an increase in arterial pressure [because more blood is being
pumped through the body]. Therefore, the mechanisms regulating sodium
balance are primarily responsible for the chronic regulation of
The kidney in blood pressure regulation by L G Navar and L L Hamm.
Finally, a very quick summary of the renin-angiotensin system, which
plays a central role in the maintenance of blood pressure levels, and
which is affected by some of the agents reponsible for increasing
Renin is produced by a number of tissues, but primarily within the
kidneys. It is released in response to one of the following stimuli:
low pressure in the renal artery, activation of the sympathetic
nervous system, low levels of sodium in the kidney tubules. Renin is
an enzyme and its effect is to catalyze the breakdown of a protein
called angiotensinogen into angiotensin I. Another enzyme called
angiotensin converting enzyme (ACE), which is found in the endothelium
(lining) of blood vessels, especially in the lungs, then chops a piece
off the angiotensin I to form angiotensin II.
Angiotensin II has a number of important effects, including:
It acts on blood vessels, making them constrict, thus increasing
resistance and blood pressure.
It stimulates the adrenal gland to release aldosterone. Aldosterone
acts on the kidneys and increases the retention of sodium and water.
It causes the pituitary gland to release vasopressin, which in turn
increases water retention by the kidneys.
It stimulates thirst centres in the brain and thus increases fluid
The effects of angiotensin II on sodium and water levels will increase
blood pressure as described in the section above on sodium.
You can see a diagram of these interactions at
Cardiovascular Physiology Concepts by Richard E. Klabunde, Ph.D.
I hope that this has answered your question to some extent. Much more
could be said on this topic, as it is very complex, with many
interacting factors. Please ask for further clarification if
Personal knowledge plus the following searches:
1. mechanisms hypertension obesity
2. dietary factors hypertension
3. licorice hypertension
4. alcohol hypertension
5. alcohol blood vessels
6. smoking hypertension
7. nicotine hypertension
8. blood pressure during exercise
9. sodium intake blood pressure
10 renin angiotensin blood pressure