Renal Effects of Nitrendipine Monotherapy in Essential Hypertension

Thananopavarn, Chalemphol; Golub, Michael S.; Eggena, Peter; Barrett, J.; Sambhi, Mohinder P.

doi:10.1097/00005344-198400067-00020

Cited by 41 publications

(14 citation statements)

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“…Short-term administration of nifedipine to normotensive subjects or hypertensive patients produced a significant increase in plasma renin activity (Aoki et al, 1976;Pedersen et al, 1979;Hiramatsu et al, 1982;Kusano et al, 1982;Leonetti et al, 1982;Kiowski et al, 1983). Results for plasma RAS components were inconsistent after treatment with nitrendipine (Thananopavarn et al, 1984;Luft et al, 1985;Pedrinelli et al, 1986), nicardipine (van Schaik et al, 1984;Elliott et al, 1985), amlodipine (Krenek et al, 2004;Lamarre-Cliche et al, 2005), or verapamil (Muiesan et al, 1982;Guthrie et al, 1983;Frohlich, 1985). Some calcium blockers such as azelnidipine may suppress the RAS although its mechanism remains unclear (Oizumi et al, 1989).…”

Section: Calcium Blockersmentioning

confidence: 99%

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

et al. 2007

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Section: Calcium Blockersmentioning

confidence: 99%

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

et al. 2007

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“…This finding suggests a sustained postdose natriuretic or diuretic effect, possibly outbalanced by a counteracting sodium-retaining state during the subsequent hours, resulting in a net unchanged 24-hour excretion. 3 ' l7~19 Isradipine induced an increased outflow of fluid from the proximal tubules, although no change in the rate of absolute proximal reabsorption of sodium was seen for the group as a whole. Nevertheless, there was a significant relationship between the degree of changes in absolute rate of proximal sodium reabsorption and changes in SBP, MBP, and DBP (see Table 2 and Figure 1).…”

mentioning

confidence: 96%

Repetitive natriuresis and blood pressure. Long-term calcium entry blockade with isradipine.

et al. 1987

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SUMMARY The long-term effects (3.5 months) of a new calcium entry blocker of the 1-4-dihydropyridine class, isradipine , on renal hemodynamics and excretional parameters were investigated in 10 essential hypertensive subjects (World Health Organization Classes I and II). Blood pressure and renal vascular resistance fell significantly (p < 0.001), and a slight increase in glomerular filtration rate and renal plasma flow was seen (p<0.05). Output of fluid from the proximal tubules, measured as clearance of lithium and uric acid, increased significantly (p<0.01 and p<0.05, respectively), and a compensatory increase in absolute reabsorption of sodium beyond the proximal tubular level accompanied by an increase in clearance of potassium was noted. A 40% increase in the resultant clearance of sodium (p<0.01) and an increase in diuresis (p<0.05) followed the morning dose of isradipine after 3.5 months of treatment. Changes in blood pressure were significantly correlated with changes in absolute proximal reabsorption of sodium (r = 0.81), excretion of sodium (r = -0.64), and diuresis (r = -0.80). Thus, the natriuretic properties of calcium entry blockers may be more important for the long-term antihypertensive effect than the vasodilator effect per se. A model for renal sodium handling following treatment with calcium entry blockers was proposed. Although a causal relationship is not implied, isradipine induced a sustained, repetitive postdose effect on proximal fluid output, net natriuresis, and diuresis, that was intimately related to the long-term blood pressureregulating response.

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“…For example, there was no exaggerated hypotensive response which could have offset an initial diuretic effect. Short-term treatment with calcium entry blockers was found to produce a moderately negative sodium balance in hypertensive patients in various other studies, but the reported effects on GFR differ from no change (de Leeuw and Brinkenhager 1984; Tananopavan et al 1985) to an increase (Baba et al 1987), as found by ourselves. Steele (1987) showed that the rise in GFR after calcium entry blockade was accentuated in isolated, perfused kidneys of spontaneous hypertensive rats, and in the kidneys of salt-sensitive Dahl rats as compared to those of salt-resistent animals.…”

Section: Different Effect In Hypertensivesmentioning

confidence: 54%

The Diuretic Effect of Calcium Entry Blockade in Normals and Hypertensive Patients.

Geyskes¹,

Schaik²,

Gaillard³

et al. 1992

Tohoku J. Exp. Med.

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Calcium entry blockers have been shown to exert hemodynamic and diuretic effects in the kidney. The diuretic effects can be demonstrated most clearly in the isolated perfused kidney, not influenced by compensatory mechanisms such as a lower blood pressure or changes of hormones. However, they can also be shown in vivo in humans. We studied the renal effects of calcium entry blockade after the first dosage and after continued oral dosages of 20 mg nicardipine tid in patients with essential hypertension and in normotensive controls. Renal function was determined during maximal free water clearance, allowing estimation of changes in "proximal" and "distal" tubular sodium reabsorption . Results showed a natriuretic effect. In the control subjects, clearance results were compatible with a decrease of proximal and distal tubular reabsorption, but in the hypertensive group natriuresis was mainly achieved by an increase of the glomerular filtration rate and a decrease of fractional distal reabsorption. In both groups the natriuresis occurred concomitantly with a lower blood pressure. The ratio plasma renin activity/plasma aldosterone concentration increased, although nicardipine did not inhibit the increase of plasma aldosterone during angiotensin II infusion. Pre-treatment with the calcium entry blocker nitrendipine enhanced the natriuretic effect of atrial natriuretic factor (ANF) in sodium replete normal volunteers. Facilitation of sodium excretion by human ANF may be an additional diuretic mechanism of calcium entry blockers.atrial natriuretic factor ; calcium entry blockade ; diuretic ; nicardipine ; sodium excretion Calcium entry blockade has been shown to exert diuretic effects. This occurs in the perfused kidney, isolated from influences of hormones and changes of arterial pressure, as well as in vivo in experimental mammals and man (Luft 1987). Despite abundant experimental demonstration of this effect, no single or principal mechanism has as yet been demonstrated. Evidence has indeed accumulated that the sodium and water excretion during calcium entry blockade has multiple causes, which even may vary among the many drugs of this class. For instance, only verapamil and diltiazem have been shown to decrease the short

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Renal Effects of Nitrendipine Monotherapy in Essential Hypertension

Cited by 41 publications

References 0 publications

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

The Intrarenal Renin-Angiotensin System: From Physiology to the Pathobiology of Hypertension and Kidney Disease

Repetitive natriuresis and blood pressure. Long-term calcium entry blockade with isradipine.

The Diuretic Effect of Calcium Entry Blockade in Normals and Hypertensive Patients.

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