1991
DOI: 10.1016/s0272-6386(12)80250-2
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Effect of a Calcium-Entry Blocker, Nicardipine, on Intrarenal Hemodynamics in Essential Hypertension

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Cited by 21 publications
(9 citation statements)
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“…Similarly, nicardipine increased renal blood flow in the present study. Although renal blood flow autoregulation is not as strict as that in the brain or heart 34), nicardipine, like other DPCs, may mainly dilate the afferent arterioles and thereby induce an increase in renal blood flow despite the reduction in renal perfusion pressure (35,36). There is also a possibility that DPCs may activate the renin-angiotensin-aldosterone system and may exacerbate proteinuria in patients with diabetes mellitus (37).…”
Section: Discussionmentioning
confidence: 99%
“…Similarly, nicardipine increased renal blood flow in the present study. Although renal blood flow autoregulation is not as strict as that in the brain or heart 34), nicardipine, like other DPCs, may mainly dilate the afferent arterioles and thereby induce an increase in renal blood flow despite the reduction in renal perfusion pressure (35,36). There is also a possibility that DPCs may activate the renin-angiotensin-aldosterone system and may exacerbate proteinuria in patients with diabetes mellitus (37).…”
Section: Discussionmentioning
confidence: 99%
“…Therefore, if specific renal determinants of the pressure-natriuresis relationship are known, then renal mechanisms of sodium sensitivity are clarified necessarily. The x-intercept, i.e., the degree of the shift along the BP axis, is determined by the sum of the pressure drop from heart to glomeruli plus the opposing pressures at glomeruli [51, 52, 56]. The main factor seems to be the preglomerular vascular resistance from heart to glomeruli, mainly due to the afferent arteriolar resistance.…”
Section: Renal Mechanisms Of Sodium Sensitivitymentioning
confidence: 99%
“…It is well known that these forms of hypertension are based on an increase in vascular resistance due to renal artery stenosis. There is ample evidence to suggest that spontaneously hypertensive rats of Kyoto strain and human essential hypertension result from increased afferent arteriolar resistance [37, 51, 56, 65, 67, 68]. …”
Section: Renal Mechanisms Of Sodium Sensitivitymentioning
confidence: 99%
“…No substantial differences have been found between Gomez’s model and the micropuncture measurements in dogs and rats [19,20,21]; moreover, filtration disequilibrium seems to be probable in healthy humans [22]. Gomez’s formulae have been used to calculate glomerular hemodynamic variables in subjects with untreated and treated essential hypertension [8,23,24,25], renovascular hypertension [26], primary aldosteronism [27], and supraventricular tachycardia [28]. However, the fact that we were interested in evaluating changes rather than absolute values of glomerular hemodynamics, together with the absence of any incongruence between the glomerular and renal variables, may justify our approach.…”
Section: Discussionmentioning
confidence: 99%