Page 229 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

!
rons of which (blue arrows) continuously blood pressure at the high levels. Chronic hyperten-
transmit sympathetic nerve impulses to the sion leads to stiffening of the carotid sinus. This may
heart to increase its activity (heart rate, con- also contribute to decreasing the sensitivity of
duction and contractility). Their effects on ves- carotid pressosensors in hypertension.
A temporary increase in venous return (e.g., after
sels are predominantly vasoconstrictive (rest- an intravenous infusion) also leads to an increase in
ing tone). The pressor area is in close contact heart action (! D, right). This mechanism is known
with more medial neurons (depressor area, as the Bainbridge reflex. The physiological signifi-
light blue area in C). The pressor and depressor cance of this reflex is, however, not entirely clear, but
areas are connected to the dorsal nuclei of the it may complement the Frank–Starling mechanism
vagus nerve (! C, green), the stimulation of (! p. 202ff.).
which reduces the heart rate and cardiac im- Hypertension
pulse conduction rate (! C, orange arrows).
Homeostatic circulatory reflexes include Hypertension is defined as a chronic increase
Cardiovascular System maintain the arterial blood pressure at a stable is consistent elevation of resting blood pres-
in the systemic arterial blood pressure. The
signals along afferent nerve tracts (! D3a/b)
general criterion for diagnosis of hypertension
that extend centrally from the pressosensors in
the aorta and carotid sinus (! C, green tracts).
sure to more than 90 mmHg diastolic (! p.
The main purpose of homeostatic control is to
206). Untreated or inadequately managed hy-
pertension results in stress and compensatory
level. Acute increases in blood pressure
hypertrophy of the left ventricle which can
heighten the rate of afferent impulses and acti-
vate the depressor area. By way of the vagus
dividuals with hypertension are also at risk for
arteriosclerosis and its sequelae (myocardial
8 nerve, parasympathetic neurons (! C, orange ultimately progress to left heart failure. In-
tract) elicit the depressor reflex response, i.e.,
they decrease the cardiac output (CO). In addi- infarction, stroke, renal damage, etc.). There-
tion, inhibition of sympathetic vessel innerva- fore, hypertension considerably shortens the
tion causes the vessels to dilate, thereby reduc- life expectancy of a large fraction of the popu-
ing the peripheral resistance (TPR; ! D4a/b). lation.
Both of these mechanisms help to lower acute The main causes of hypertension are (a) increased
increases in blood pressure. Conversely, an extracellular fluid (ECF) volume with increased
acute drop in blood pressure leads to activation venous return and therefore increased cardiac out-
of pressor areas, which stimulates a rise in CO put (volume hypertension) and (b) increased total pe-
and TPR as well as venous vasoconstriction ripheral resistance (resistance hypertension). As hy-
pertension always leads to vascular changes result-
(! C, blue tracts), thereby raising the blood ing in increased peripheral resistance, type a hyper-
pressure back to normal. tension eventually proceeds to type b which, regard-
Due to the fast adaptation of pressosensors less of how it started, ends in a vicious circle.
(differential characteristics, ! p. 312ff.), these The ECF volume increases when more NaCl (and
regulatory measures apply to acute changes in water) is absorbed than excreted. The usually high in-
blood pressure. Rising, for example, from a take of dietary salt may therefore play a role in the
supine to a standing position results in rapid development of essential hypertension (primary
hypertension), the most common type of hyperten-
redistribution of the blood volume. Without sion, at least in patients sensitive to salt. Volume hy-
homeostatic control (orthostatic reflex; pertension can even occur when a relatively low salt
! p. 204), the resulting change in venous re- intake can no longer be balanced. This can occur in
turn would lead to a sharp drop in arterial renal insufficiency or when an adrenocortical tumor
blood pressure. The circulatory centers also re- produces uncontrolled amounts of aldosterone, re-
+
spond to falling PO 2 or rising PCO 2 in the blood sulting in Na retention.
Other important cause of hypertension is
(cross-links from respiratory center) to raise pheochromocytoma, a tumor that secretes epi-
the blood pressure as needed.
nephrine and norepinephrine and therefore raises
In individuals with chronic hypertension, the input the CO and TPR. Renal hypertension can occur due
from the pressosensors is normal because they are to renal artery stenosis and renal disease. This results
fully adapted. Therefore, circulatory control centers in the increased secretion of renin, which in turn
216 cannot respond to and decrease the high pressures. raises the blood pressure via the renin–angiotensin–
On the contrary, they may even help to “fix” the aldosterone (RAA) system (! p. 184).
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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