Calcium Antagonists in the Treatment of Hypertension

Ram, Chirag; Featherston, W. E.

doi:10.1378/chest.93.6.1251

Cited by 9 publications

(2 citation statements)

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“…270, 271 Some agents act directly on cardiac muscle to suppress pacemaker activity. 272, 273 Even with dihydropyridine CCBs, which have less of an effect on the pacemaker, reflex tachycardia is usually absent and the heart rate may decrease. 271 Of course, reflex tachycardia occurs when a potent CCB like nifedipine is administered and rapidly lowers blood pressure.…”

Section: Antihypertensive Agents and The Central Mechanism Of Blood Pmentioning

confidence: 99%

The central mechanism underlying hypertension: a review of the roles of sodium ions, epithelial sodium channels, the renin–angiotensin–aldosterone system, oxidative stress and endogenous digitalis in the brain

et al. 2011

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The central nervous system has a key role in regulating the circulatory system by modulating the sympathetic and parasympathetic nervous systems, pituitary hormone release, and the baroreceptor reflex. Digoxin- and ouabain-like immunoreactive materials were found >20 years ago in the hypothalamic nuclei. These factors appeared to localize to the paraventricular and supraoptic nuclei and the nerve fibers at the circumventricular organs and supposed to affect electrolyte balance and blood pressure. The turnover rate of these materials increases with increasing sodium intake. As intracerebroventricular injection of ouabain increases blood pressure via sympathetic activation, an endogenous digitalis-like factor (EDLF) was thought to regulate cardiovascular system-related functions in the brain, particularly after sodium loading. Experiments conducted mainly in rats revealed that the mechanism of action of ouabain in the brain involves sodium ions, epithelial sodium channels (ENaCs) and the renin–angiotensin–aldosterone system (RAAS), all of which are affected by sodium loading. Rats fed a high-sodium diet develop elevated sodium levels in their cerebrospinal fluid, which activates ENaCs. Activated ENaCs and/or increased intracellular sodium in neurons activate the RAAS; this releases EDLF in the brain, activating the sympathetic nervous system. The RAAS promotes oxidative stress in the brain, further activating the RAAS and augmenting sympathetic outflow. Angiotensin II and aldosterone of peripheral origin act in the brain to activate this cascade, increasing sympathetic outflow and leading to hypertension. Thus, the brain Na+–ENaC–RAAS–EDLF axis activates sympathetic outflow and has a crucial role in essential and secondary hypertension. This report provides an overview of the central mechanism underlying hypertension and discusses the use of antihypertensive agents.

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Section: Antihypertensive Agents and The Central Mechanism Of Blood Pmentioning

confidence: 99%

The central mechanism underlying hypertension: a review of the roles of sodium ions, epithelial sodium channels, the renin–angiotensin–aldosterone system, oxidative stress and endogenous digitalis in the brain

et al. 2011

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“…It is now well known that calcium antagonists, which block transmembrane calcium influx into vascular smooth muscle cells and reduce vascular tone, are useful for the treatment of hypertension [1][2][3][4]. Furthermore, it has been demonstrated that these drugs increase renal blood flow (RBF) glomerular filtration rate and urinary excretion of water and sodium and that the renal hemo dynamic and excretory functions are most apparent un der conditions in which basal renal vascular tone is enhanced [1,[5][6][7], In renin-dependent phase of two-kidney, one-clip renovascular hypertension, several reports demonstrated the antihypertensive effects of calcium antagonists [8][9][10], Huang [9] reported that nifedipine, a calcium antagonist, which has the most vascular selectiv ity of all calcium antagonists, enhanced glomerular fil tration and suppressed the reabsorption of sodium and water, which contribute to the antihypertensive effects.…”

Section: Introductionmentioning

confidence: 99%

Effects of Nifedipine on Renal Cortical and Medullary Blood Flow in Two-Kidney, One-Clip Renovascular Hypertension in Rabbits

et al. 1990

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The effects of nifedipine, a calcium antagonist, on blood pressure and renal regional blood flow were investigated in two-kidney, one-clip renovascular hypertensive rabbits. At 1 week after left renal artery constriction, in the constricted group, systemic blood pressure (BP) significantly rose with the elevation of plasma renin activity (PRA). In both kidneys, renal vascular resistance (RVR) on the constricted group was significantly increased as compared to that in the control group. In the clipped kidney, total renal blood flow (RBF) and renal cortical blood flow (RCBF) of the constricted group were significantly decreased, while renal medullary blood flow (RMBF) remained at the control value. In the nonclipped kidney, RBF and RCBF of the constricted group did not significantly change, and RMBF was significantly increased as compared to that of the control group. After administration of nifedipine for 1 week (1.0 mg/kg/day), BP in the constricted group was decreased to the control level and PRA in both groups was increased. The percent change of BP in the constricted group was significantly decreased and the percent change of PRA in the constricted group was significantly increased as compared to those in the control group. Nifedipine increased RBF, RCBF and RMBF and decreased RVR of both kidneys in each group. In the nonclipped kidney, the percent change of RBF, RCBF and RMBF of the constricted group was significantly increased and the percent change of RVR was significantly decreased as compared to those of the control group. In the clipped kidney, only the percent change of RBF of the constricted group was significantly lower than that in the control group. The percent change of RVR, RCBF and RMBF were almost at the control levels. In both groups, there were no significant differences between the percent change of RCBF and RMBF of each kidney. These results indicated that nifedipine has an antihypertensive effect associated with a decrease in RVR and an increase in RBF and renal regional blood flow, which are mainly observed in the nonclipped kidney, in the renin-dependent phase of two-kidney, one-clip renovascular hypertensive rabbits. It is suggested that nifedipine did not cause the shift of the intrarenal blood flow distribution.

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How Urgent Is 'Urgent' Hypertension?

Ferguson¹

1989

Arch Intern Med

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Calcium Antagonists in the Treatment of Hypertension

Cited by 9 publications

References 0 publications

The central mechanism underlying hypertension: a review of the roles of sodium ions, epithelial sodium channels, the renin–angiotensin–aldosterone system, oxidative stress and endogenous digitalis in the brain

The central mechanism underlying hypertension: a review of the roles of sodium ions, epithelial sodium channels, the renin–angiotensin–aldosterone system, oxidative stress and endogenous digitalis in the brain

Effects of Nifedipine on Renal Cortical and Medullary Blood Flow in Two-Kidney, One-Clip Renovascular Hypertension in Rabbits

How Urgent Is 'Urgent' Hypertension?

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