Blood pressure in hypertension

Calcium channel blockers cause more pronounced lowering of blood pressure in hypertensive patients than in normotensive individuals. Generally, all calcium channel blockers cause an immediate increase in PRA during acute treatment in patients having hypertension but PRA is normalized during chronic treatment despite the sustained decrease in blood pressure. These agents also do not generally produce sodium and water retention, unlike the conventional vasodilators. This is because they produce diuretic effects by direct actions on the kidney. 

Verapamil (Table 1), the first slow channel calcium blocker synthesized to selectively inhibit the transmembrane influx of calcium ions into cells, lowers blood pressure in hypertensive patients having good organ perfusion particularly with increased renal blood flow. Sustained-release verapamil for once a day dosing is available for the treatment of hypertension. Constipation is a prominent side effect. Headache, dizziness, and edema are frequent and verapamil can sometimes cause AV conduction disturbances and AV block. Verapamil should not be used in combination with -adrenoceptor blockers because of the synergistic negative effects on heart rate and contractile force. 

Angiotensin converting enzyme (ACE) plays a central role in cardiovascular hemostasis. Its major function is the generation of angiotensin (ANG) II from ANGI and the degradation of bradykinin. Both peptides have profound impact on the cardiovascular system and beyond. ACE inhibitors are used to decrease blood pressure in hypertensive patients, to improve cardiac function, and to reduce work load of the heart in patients with cardiac failure. 

Lowers blood pressure in hypertensive patients by inhibition of peptidyl dipeptidase... 

NO release is considerably slowed down when lrans- Ru(Cl) (NO) (cyclam)] is reduced (Scheme 5.8(b)). It has also been observed [204] that the reduction in blood pressure in hypertensive Wistar rats is more prolonged by the administration of cyclam-NO than when SNP is administered. This suggests that the metal cyclam NO complex could be used as a long lasting vasodilator [214]. 

It is claimed that chronic deficiency of arachidonic acid can lead to a number of medical problems that can be overcome by supplementation of a normal diet with evening primrose oil. Supplementation is claimed to lead to an alleviation of eczema reduction in premenstrual tension and breast pain during menstruation improvement in some chronic inflammatory and autoimmune diseases reduction in blood pressure in hypertensive patients and reduction in blood cholesterol levels. As might be expected, these claims are controversial, but they serve to illustrate how basic biochemical information can lead to a considerable lay interest in a subject. 

Hata Y, Yamamoto M, Ohni M, Nakajima K, Nakamura Y, Takano T. (1996) A placebo-controlled study of the effect of sour milk on blood pressure in hypertensive subjects. Am J Clin Nutr 64 161-11. ... 

Adrenergic neurone blocking activity is increased when substituents are introduced into the ortho- and para-positions of benzylguanidine (Table 3.18) active compounds include the bromo (a particularly close analogue of bretylium), chloro and trifluoromethyl derivatives (LIV, R = 2-Br, 2-Cl, 2- and 4-CFa) [140, 141, 239, 242]. The 4-trifluoromethyl derivative, which has a relaxing effect on the nictitating membrane of cats comparable in intensity and duration to bethanidine, also decreased blood pressure in hypertensive dogs [141]. Certain... 

Possible uses. Arteriolar vasodilators are given to lower blood pressure in hypertension (p. 312), to reduce cardiac work in angina pectoris (p. 308), and to reduce ventricular afterload (pressure load) in cardiac failure (p. 132). Venous vasodilators are used to reduce venous filling pressure (preload) in angina pectoris (p. 308) or cardiac failure (p. 132). 

Sodium nitroprusside is a powerful, instantaneous-acting intravenous drug used to lower blood pressure in hypertensive crises. The hypotensive effect is caused by peripheral vasodilation resulting from a direct effect on both arterial and venous vessels. 

Blood pressure in a hypertensive patient is controlled by the same mechanisms that are operative in normotensive subjects. Regulation of blood pressure in hypertensive patients differs from healthy patients in that the baroreceptors and the renal blood volume-pressure control systems appear to be "set" at a higher level of blood pressure. All antihypertensive drugs act by interfering with these normal... 

Dietary sodium restriction has been known for many years to decrease blood pressure in hypertensive patients. With the advent of diuretics, sodium restriction was thought to be less important. However, there is now general agreement that dietary control of blood pressure is a relatively nontoxic therapeutic measure and may even be preventive. Even modest dietary sodium restriction lowers blood pressure (though to varying extents) in many hypertensive persons. 

Propranolol inhibits the stimulation of renin production by catecholamines (mediated by receptors). It is likely that propranolol s effect is due in part to depression of the renin-angiotensin-aldosterone system. Although most effective in patients with high plasma renin activity, propranolol also reduces blood pressure in hypertensive patients with normal or even low renin activity. Beta blockers might also act on peripheral presynaptic adrenoceptors to reduce sympathetic vasoconstrictor nerve activity. 

Weight reduction even without sodium restriction has been shown to normalize blood pressure in up to 75% of overweight patients with mild to moderate hypertension. Regular exercise has been shown in some but not all studies to lower blood pressure in hypertensive patients. 

Potent peptide antagonists of the action of Ang II are available. The best-known of these is the partial agonist, saralasin. Saralasin lowers blood pressure in hypertensive patients but may elicit pressor responses, particularly when circulating Ang II levels are low. Because it must be administered intravenously, saralasin is used only for investigation of renin-dependent hypertension and other hyperreninemic states. 

A link between heavier alcohol consumption (more than three drinks per day) and hypertension has been firmly established in epidemiologic studies. Alcohol is estimated to be responsible for approximately 5% of cases of hypertension, making it one of the most common causes of reversible hypertension. This association is independent of obesity, salt intake, coffee drinking, and cigarette smoking. A reduction in alcohol intake appears to be effective in lowering blood pressure in hypertensives who are also heavy drinkers the hypertension seen in this population is also responsive to standard blood pressure medications. 

The supplementation with an oral dose of 1 g of quercetin for 1 month to healthy normotensive subjects has been recently compared to placebo, showing no differences in selected cardiovascular risk factors including blood pressure [102]. However, these data do not exclude an antihypertensive effect of quercetin in patients with essential hypertension. In fact, a diet rich in fruit and vegetables (and presumably rich in flavonoids) lowered blood pressure in hypertensive but not in normotensive subjects [156,157]. 

Edwards RL, Lyon T, Litwin SE, Rabovsky A, Symons JD, Jalili T. 2007. Quercetin reduces blood pressure in hypertensive subjects. J Nutr 137 2405-2411. 

By the use of specific enzymes, studies have been made in an attempt to classify the pressor substances in experimental hypertension. If a specific enzyme lowered blood pressure in hypertensive animals and not in normal ones, it was assumed that the substrate of that enzyme was attacked, and therefore contributed to the hypertension. Such assumptions, while not wholly valid, nevertheless pointed to certain substances as possibly concerned in hypertension. 

Sipola, M., Finckenberg, P., Korpela, R., Vapaatalo, H., and Nurminen, M.-L. 2002a. Effect of long-term intake of milk products on blood pressure in hypertensive rats. J. Dairy Res. 69, 103-111. 

All the clinically available (J-blockers are competitive antagonists. Nonselective [3-blockers act at both (3 and (32 receptors, whereas car-dioselective ( -antagonists primarily block 3i receptors. These drugs also differ in intrinsic sympathomimetic activity, in central nervous system (CNS) effects, and in pharmacokinetics (Figure 7.5). Although all (3-blockers lower blood pressure in hypertension, they do not induce postural hypotension because the a-adrenoceptors remain functional therefore, normal sympathetic control of the vasculature is maintained. P-blockers are also effective in treating angina, cardiac arrhythmias,... 

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