Hemodynamic and renin responses to nifedipinein renovascular hypertension

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

We investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics in twelve patients who had severe hypertension (diastolic values averaging 114 mm Hg) with unilateral renal artery stenosis (angiography) and hyperreninemia. Plasma renin activity was determined from blood samples drawn from the aorta and from both renal veins, so that "ischemic lateralization" could be evaluated through appropriately derived indexes. Nifedipine promptly and significantly lowered aortic pressure in all patients. At 30 minutes maximal circulatory responses were recorded, which consisted of a 22% decrease in mean aortic pressure (from an average of 144.6±15 mm Hg to an average of 113±11 mm Hg), a 44% reduction of systemic vascular resistance (from 2162±540 dynes·sec·cm-5 to 1205±279 dynes · sec · cm-5), a 33% rise in cardiac index (from 2920±970 ml/min/m2 to 3875±986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 minutes of continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in persons with primary hypertension with similar levels of blood pressure. After nifedipine was given, renin activity of the systemic blood rose significantly, because of a potentiated release from the kidney with arterial stenosis. This effect, which was inferred as being due to further reduction of the renal perfusion pressure, improved the significance of "ischemic lateralization" indexes and supported the diagnosis of renovascular hypertension in all cases. It is suggested that nifedipine may be regarded not only as an additional diagnostic tool but also as an effective antihypertensive agent for this disorder, at least for short periods of time. This action is in contrast to the previous suggestion that nifedipine is substantially more effective in low-renin rather than in high-renin hypertension. Indeed, in the present population, as in persons with primary hypertension, the extent of the reduction of blood pressure correlates with the baseline values of systemic vascular resistance and not with renin levels.

Original languageEnglish
Pages (from-to)353-356
Number of pages4
JournalAmerican Heart Journal
Volume119
Issue number2 PART 1
DOIs
Publication statusPublished - 1990

Fingerprint

Renovascular Hypertension
Renin
Nifedipine
Hemodynamics
Hypertension
Vascular Resistance
Arterial Pressure
Blood Pressure
Kidney
Renal Artery Obstruction
Renal Veins
Antihypertensive Agents
Aorta
Angiography
Pathologic Constriction
Perfusion
Pressure
Population

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Hemodynamic and renin responses to nifedipinein renovascular hypertension. / Fiorentini, Cesare; Galli, Claudia; Tamborini, Gloria; Tosi, Elena; Riva, Stefania.

In: American Heart Journal, Vol. 119, No. 2 PART 1, 1990, p. 353-356.

Research output: Contribution to journalArticle

@article{20bd14372abb41578ff206faa901f42e,
title = "Hemodynamic and renin responses to nifedipinein renovascular hypertension",
abstract = "We investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics in twelve patients who had severe hypertension (diastolic values averaging 114 mm Hg) with unilateral renal artery stenosis (angiography) and hyperreninemia. Plasma renin activity was determined from blood samples drawn from the aorta and from both renal veins, so that {"}ischemic lateralization{"} could be evaluated through appropriately derived indexes. Nifedipine promptly and significantly lowered aortic pressure in all patients. At 30 minutes maximal circulatory responses were recorded, which consisted of a 22{\%} decrease in mean aortic pressure (from an average of 144.6±15 mm Hg to an average of 113±11 mm Hg), a 44{\%} reduction of systemic vascular resistance (from 2162±540 dynes·sec·cm-5 to 1205±279 dynes · sec · cm-5), a 33{\%} rise in cardiac index (from 2920±970 ml/min/m2 to 3875±986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 minutes of continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in persons with primary hypertension with similar levels of blood pressure. After nifedipine was given, renin activity of the systemic blood rose significantly, because of a potentiated release from the kidney with arterial stenosis. This effect, which was inferred as being due to further reduction of the renal perfusion pressure, improved the significance of {"}ischemic lateralization{"} indexes and supported the diagnosis of renovascular hypertension in all cases. It is suggested that nifedipine may be regarded not only as an additional diagnostic tool but also as an effective antihypertensive agent for this disorder, at least for short periods of time. This action is in contrast to the previous suggestion that nifedipine is substantially more effective in low-renin rather than in high-renin hypertension. Indeed, in the present population, as in persons with primary hypertension, the extent of the reduction of blood pressure correlates with the baseline values of systemic vascular resistance and not with renin levels.",
author = "Cesare Fiorentini and Claudia Galli and Gloria Tamborini and Elena Tosi and Stefania Riva",
year = "1990",
doi = "10.1016/S0002-8703(05)80027-4",
language = "English",
volume = "119",
pages = "353--356",
journal = "American Heart Journal",
issn = "0002-8703",
publisher = "Mosby Inc.",
number = "2 PART 1",

}

TY - JOUR

T1 - Hemodynamic and renin responses to nifedipinein renovascular hypertension

AU - Fiorentini, Cesare

AU - Galli, Claudia

AU - Tamborini, Gloria

AU - Tosi, Elena

AU - Riva, Stefania

PY - 1990

Y1 - 1990

N2 - We investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics in twelve patients who had severe hypertension (diastolic values averaging 114 mm Hg) with unilateral renal artery stenosis (angiography) and hyperreninemia. Plasma renin activity was determined from blood samples drawn from the aorta and from both renal veins, so that "ischemic lateralization" could be evaluated through appropriately derived indexes. Nifedipine promptly and significantly lowered aortic pressure in all patients. At 30 minutes maximal circulatory responses were recorded, which consisted of a 22% decrease in mean aortic pressure (from an average of 144.6±15 mm Hg to an average of 113±11 mm Hg), a 44% reduction of systemic vascular resistance (from 2162±540 dynes·sec·cm-5 to 1205±279 dynes · sec · cm-5), a 33% rise in cardiac index (from 2920±970 ml/min/m2 to 3875±986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 minutes of continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in persons with primary hypertension with similar levels of blood pressure. After nifedipine was given, renin activity of the systemic blood rose significantly, because of a potentiated release from the kidney with arterial stenosis. This effect, which was inferred as being due to further reduction of the renal perfusion pressure, improved the significance of "ischemic lateralization" indexes and supported the diagnosis of renovascular hypertension in all cases. It is suggested that nifedipine may be regarded not only as an additional diagnostic tool but also as an effective antihypertensive agent for this disorder, at least for short periods of time. This action is in contrast to the previous suggestion that nifedipine is substantially more effective in low-renin rather than in high-renin hypertension. Indeed, in the present population, as in persons with primary hypertension, the extent of the reduction of blood pressure correlates with the baseline values of systemic vascular resistance and not with renin levels.

AB - We investigated the acute effects of nifedipine (10 mg orally) on renin and systemic hemodynamics in twelve patients who had severe hypertension (diastolic values averaging 114 mm Hg) with unilateral renal artery stenosis (angiography) and hyperreninemia. Plasma renin activity was determined from blood samples drawn from the aorta and from both renal veins, so that "ischemic lateralization" could be evaluated through appropriately derived indexes. Nifedipine promptly and significantly lowered aortic pressure in all patients. At 30 minutes maximal circulatory responses were recorded, which consisted of a 22% decrease in mean aortic pressure (from an average of 144.6±15 mm Hg to an average of 113±11 mm Hg), a 44% reduction of systemic vascular resistance (from 2162±540 dynes·sec·cm-5 to 1205±279 dynes · sec · cm-5), a 33% rise in cardiac index (from 2920±970 ml/min/m2 to 3875±986 ml/min/m2). These effects were still evident, although somewhat tempered, after 180 minutes of continuous monitoring; they were qualitatively and quantitatively similar to those reported by some authors in persons with primary hypertension with similar levels of blood pressure. After nifedipine was given, renin activity of the systemic blood rose significantly, because of a potentiated release from the kidney with arterial stenosis. This effect, which was inferred as being due to further reduction of the renal perfusion pressure, improved the significance of "ischemic lateralization" indexes and supported the diagnosis of renovascular hypertension in all cases. It is suggested that nifedipine may be regarded not only as an additional diagnostic tool but also as an effective antihypertensive agent for this disorder, at least for short periods of time. This action is in contrast to the previous suggestion that nifedipine is substantially more effective in low-renin rather than in high-renin hypertension. Indeed, in the present population, as in persons with primary hypertension, the extent of the reduction of blood pressure correlates with the baseline values of systemic vascular resistance and not with renin levels.

UR - http://www.scopus.com/inward/record.url?scp=0025051888&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025051888&partnerID=8YFLogxK

U2 - 10.1016/S0002-8703(05)80027-4

DO - 10.1016/S0002-8703(05)80027-4

M3 - Article

VL - 119

SP - 353

EP - 356

JO - American Heart Journal

JF - American Heart Journal

SN - 0002-8703

IS - 2 PART 1

ER -