Manual Essential Hypertension: Calcium Mechanisms and Treatment

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An effective and inexpensive way of reducing venous pressure and cardiac output is by using drugs that reduce blood volume.

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These drugs diuretics act on the kidney to enhance sodium and water excretion. Reducing blood volume not only reduces central venous pressure, but even more importantly, reduces cardiac output by the Frank-Starling mechanism due to the reduction in ventricular preload.

An added benefit of these drugs is that they reduce systemic vascular resistance with long-term use. Many antihypertensive drugs have their primary action on systemic vascular resistance.

Recognizing and treating two types of long-term vasoconstriction in hypertension.

Some of these drugs produce vasodilation by interfering with sympathetic adrenergic vascular tone sympatholytics or by blocking the formation of angiotensin II or its vascular receptors. Other drugs are direct arterial dilators, and some are mixed arterial and venous dilators. Although less commonly used because of a high incidence of side effects, there are drugs that act on regions in the brain that control sympathetic autonomic outflow. One of the two mechanisms also sustains diastolic hypertension in the experimental and clinical forms of renovascular hypertension and primary aldosteronism.

Thus, both experimentally and clinically, at the polar extremes of the range of plasma renin values, one of the two mechanisms predominates: it is possible that, in the medium range of renin values, both mechanisms contribute to vasoconstriction. In our proposed unifying, analytic model, arteriolar vasoconstriction is associated with increased intracellular calcium and decreased magnesium levels in vascular smooth muscle.

In the vasoconstriction consequent to sodium-volume expansion, cytosolic calcium is increased by an increased membrane influx. In renin-mediated vasoconstriction, receptor-operated channels mobilize cytosolic calcium instead from intracellular stores. Hypertens Res ; 31 : — Genome-wide association study of blood pressure and hypertension.

Hypertension - Clinical Presentation

Nat Genet ; 41 : — A large-scale genome-wide association study of Asian populations uncovers genetic factors influencing eight quantitative traits. Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

Nature ; : — Hypertension ; 56 : — Mice lacking hypertension candidate gene ATP2B1 in vascular smooth muscle cells show significant blood pressure elevation. Hypertension ; 59 : — ATP2B1 and blood pressure: from associations to pathophysiology.


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Circ J ; 70 : — Angiotensin II regulates liver regeneration via type 1 receptor following partial hepatectomy in mice.

The Pharmacologic Treatment of Systemic Hypertension - Antihypertensive Drugs

Biol Pharm Bull ; 31 : — A simple method of isolating mouse aortic endothelial cells. J Atheroscler Thromb ; 12 : — Persistence of anti-hypertensive effect after 'missed doses' of calcium antagonist with long amlodipine vs. Br J Clin Pharmacol ; 41 : 83— Intravenous nicardipine: its use in the short-term treatment of hypertension and various other indications.

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Role of natural herbs in the treatment of hypertension Tabassum N, Ahmad F - Phcog Rev

Gen Pharmacol ; 34 : — The pharmacokinetics of amlodipine in healthy volunteers after single intravenous and oral doses and after 14 repeated oral doses given once daily. Br J Clin Pharmacol ; 22 : 21— Amlodipine reduces AngII-induced aortic aneurysms and atherosclerosis in hypercholesterolemic mice. Depressor effect of chymase inhibitor in mice with high salt-induced moderate hypertension. L-type CaV1.

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Physiol Rev ; 94 : — Calcium-antagonist drugs. N Engl J Med ; : — Hypertension ; 40 : — Circ Res ; 94 : e97— Angiotensin II causes endothelial-dependent increase in expression of Ca V 1.

Eur J Pharmacol ; : — Control of vascular tone in isolated mesenteric arterial segments from hypertensive patients. Br J Pharmacol ; : — Harraz OF, Altier C.

Front Cell Neurosci ; 8 : Identification of PDZ domain containing proteins interacting with 1. Vascular nitric oxide: Beyond eNOS. J Pharmacol Sci ; : 83— Regulation of vascular tone in animals overexpressing the sarcolemmal calcium pump.