Regulation of arterial pressure

Ohm s law, which correlates the effects of blood pressure and vascular resistance on blood flow through a vessel (Q = AP/R), may also be applied to blood flow through the entire systemic circulation, or cardiac output  

Mean arterial pressure = cardiac output x total peripheral resistance 

The sympathetic system innervates most tissues in the heart including the SA node, AV node, and ventricular muscle. Sympathetic stimulation causes an increase in HR as well as an increase in ventricular contractility, which 

Parasympathetic Sympathetic — Venous activity activity return 

Sympathetic Vasoactive Local metabolic activity substances activity 

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Vasopressin also plays an important role in the short-term regulation of arterial pressure by its vasoconstrictor action. It increases total peripheral resistance when infused in doses less than those required to produce maximum urine concentration. Such doses do not normally increase arterial pressure because the vasopressor activity of the peptide is buffered by a reflex decrease in cardiac output. When the influence of this reflex is removed, eg, in shock, pressor sensitivity to vasopressin is greatly increased. Pressor sensitivity to vasopressin is also enhanced in patients with idiopathic orthostatic hypotension. Higher doses of vasopressin increase blood pressure even when baroreceptor reflexes are intact. 

The angiotensin-converting enzyme catalyses two reactions which are supposed to play an important role in the regulation of arterial pressure (1) conversion of angiotensin I, which is an inactive decapeptide, into angiotensin II, an octapeptide with a very potent vasoconstrictor activity ... 

The sympathetic adrenergic nervous system plays a major role in the regulation of arterial pressure. Activation of these nerves to the heart increases the heart rate (positive chronotropy), contractility (positive inotropy), and velocity of electrical impulse conduction (positive dromotropy). Within the medulla are located preganglionic sympathetic excitatory neurons, which travel from the spinal cord to the ganglia. They have significant basal activity, which generates a level of sympathetic tone to the heart and vasculature even under basal conditions. The sympathetic ... 

Burattini, R., Reale, R, Borgdorff, R, and Westerhof, N. 1987. Dynamic model of the short-term regulation of arterial pressure in the cat. Med. Biol. Eng. Comput. 25 269-276. 

Laragh, J.H. Renin, angiotensin, aldosterone, and hormonal regulation of arterial pressure and salt balance introductory remarks. Fed. Proc. 

Figure 15.5 Effects of sympathetic and parasympathetic nervous activity on mean arterial pressure. The parasympathetic nervous system innervates the heart and therefore influences heart rate and cardiac output. The sympathetic nervous system innervates the heart and veins and thus influences cardiac output. This system also innervates the arterioles and therefore influences total peripheral resistance. The resulting changes in cardiac output and total peripheral resistance regulate mean arterial pressure.

The linkage HA-NO-blood pressure was also demonstrated in rats that had been administered HA intracerebroventricularly into a particular forebrain area, in doses ranging from 0.01 to 0.5 mg . A dose-dependent increase in NO release and a concomitant decrease in arterial blood pressure promoted the understanding of the role of NO in central regulation of blood pressure, and further substantiated the contention that endogenous HA may serve as a source of NO. The intracranial administration of HA into rats was also used to demonstrate the existence of an NO-dopamine pathway that is likely to be involved in control of blood pressure . 

NO has a significant effect on vascular smooth muscle tone and blood pressure. Numerous endothelium-dependent vasodilators, such as acetylcholine and bradykinin, act by increasing intracellular calcium levels, which induces NO synthesis (Figure 19-2). Mice with a knockout mutation in the eNOS gene display increased vascular tone and elevated mean arterial pressure, indicating that eNOS is a fundamental regulator of blood pressure. The effects of vasopressor drugs are increased by inhibition of NOS. 

Stella L, de Novellis V, Marabese I, Berrino L, Maione S, Filippelli A, Rossi F (1998) The role of A, adenosine receptors in central regulation of arterial blood pressure. Br J Pharmacol 125(3) 437-440... 

Long-term control of arterial pressure has been attributed to the kidney by virtue of its ability to couple the regulation of blood volume to the maintenance of sodium and water balance by the mechanisms of pressure natriuresis and dieresis [31]. In the presence of a... 

Wolf, W. A., Kuhn, D. M., and Lovenberg, W., Serotonin and central regulation of arterial blood pressure, in Serotonin and the Cardiovascular System, VanHoutte, P. M., Ed., Raven Press, New York, 1985, 63-73. 

No explanation of hypertension will ever be complete without considering the role of the kidney. It has been postulated that the kidney may be the main controller of arterial pressure by means of its function to regulate fluid volume in the body. Higher sympathetic activity (NE levels) sustains blood pressure by inhibiting renal Na+ excretion. This hypothesis would explain the usefulness of natriuretic (Na+ excreting) diuretic effects. 

Cholewa, B. C., C. J. Meister, and D. L. Mattson. 2005. Importance of the renin-angiotensin system in the regulation of arterial blood pressure in conscious mice and rats. Acta Physiologica Scandinavica 183 309-320. 

The renin-angiotensin system plays a major role in the regulation of arterial blood pressure. Modest increases in plasma concentrations of Angll. When a single moderate dose of Angll is injected intravenously, systemic blood pressure begins to rise within seconds, peaks rapidly, and returns to... 

Knot, H.J. and Nelson, M.T. (1998a) Regulation of arterial diameter and calcium in cerebral arteries of rat by membrane potential and intravascular pressure. Journal of Physiology, (In Press)... 

Following ehemodenervation in the anesthetized animal, systemic hypoxia produces a powerful increase in sympathetic discharge and arterial blood pressure (61-63). That this is mediated in the brainstem is indicated by a similar effect of the injeetion of hypoxie saline or cyanide (NaCN) in the right vertebral artery of the anesthetized deafferented cat (64). This response has been shown to be mediated by reticulospinal vasomotor neurons located in the RVLM (63,65,66) that appear to be essential for the generation and reflex regulations of arterial blood pressure (67). 

Aldosterone acts on the distal tubule of the nephron to increase sodium reabsorption. The mechanism of action involves an increase in the number of sodium-permeable channels on the luminal surface of the distal tubule and an increase in the activity of the Na+-K+ ATPase pump on the basilar surface of the tubule. Sodium diffuses down its concentration gradient out of the lumen and into the tubular cells. The pump then actively removes the sodium from cells of the distal tubule and into the extracellular fluid so that it may diffuse into the surrounding capillaries and return to the circulation. Due to its osmotic effects, the retention of sodium is accompanied by the retention of water. In other words, wherever sodium goes, water follows. As a result, aldosterone is very important in regulation of blood volume and blood pressure. The retention of sodium and water expands the blood volume and, consequently, increases mean arterial pressure. 

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