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Effect of angiotensin-converting enzyme two-week inhibition on renal angiotensin II receptors and renal vascular reactivity in SHR.
J Mol Cell Cardiol. 1997 Feb; 29(2):813-22.JM

Abstract

We recently reported that intrarenal vascular AT1 angiotensin II (ANG II) receptors are major determinants of the increased vascular resistance and reactivity to ANG II observed in the kidney of spontaneously hypertensive rats (SHR). We decided to test the hypothesis that, by modifying plasma ANG II levels by inhibiting the ANG II-converting enzyme (ACE) with captopril, we would modify intrarenal ANG II receptors, and therefore the renal vascular response to ANG II. Two approaches were taken: (1) radioligand binding assays were performed on membrane preparations of purified renal microvessels and glomeruli, with displacement of 125I-[Sar-Ile8]-ANG II by specific non-peptide antagonists of AT (losartan) and AT2 (PD 123319): (2) dose-response curves to ANG II on the isolated perfused kidney were studied. Two weeks of captopril treatment significantly reduced blood pressure (BP) and relative heart weight, and increased plasma renin activity. The binding assays showed that renal microvessels and glomeruli expressed a single receptor population (AT1) for ANG II. The density of glomerular AT1 was not modulated by captopril treatment (600 +/- 174 v 573 +/- 97 fmol/mg protein in non-treated and treated SHR respectively); however. AT1 density on the intrarenal arteries increased 3-fold (55 +/- 20 v 154 +/- 30 fmol/mg protein in non-treated and treated SHR respectively. P < 0.05). Experiments with isolated perfused kidneys demonstrated that captopril did not improve the compliance of intrarenal vessels to high flow but increased their reactivity to ANG II (ED50 = 18 nM v 0.5 pM, P < 0.01). We conclude that treatment with an ACE inhibitor increases vascular reactivity to ANG II which may be mediated by an upregulation of renal vascular ANG II receptors.

Authors+Show Affiliations

Laboratory of Experimental Hypertension and Vasoactive Peptides, Clinical Research Institute of Montreal, Quebec, Canada.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9140837

Citation

Haddad, G, and R Garcia. "Effect of Angiotensin-converting Enzyme Two-week Inhibition On Renal Angiotensin II Receptors and Renal Vascular Reactivity in SHR." Journal of Molecular and Cellular Cardiology, vol. 29, no. 2, 1997, pp. 813-22.
Haddad G, Garcia R. Effect of angiotensin-converting enzyme two-week inhibition on renal angiotensin II receptors and renal vascular reactivity in SHR. J Mol Cell Cardiol. 1997;29(2):813-22.
Haddad, G., & Garcia, R. (1997). Effect of angiotensin-converting enzyme two-week inhibition on renal angiotensin II receptors and renal vascular reactivity in SHR. Journal of Molecular and Cellular Cardiology, 29(2), 813-22.
Haddad G, Garcia R. Effect of Angiotensin-converting Enzyme Two-week Inhibition On Renal Angiotensin II Receptors and Renal Vascular Reactivity in SHR. J Mol Cell Cardiol. 1997;29(2):813-22. PubMed PMID: 9140837.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of angiotensin-converting enzyme two-week inhibition on renal angiotensin II receptors and renal vascular reactivity in SHR. AU - Haddad,G, AU - Garcia,R, PY - 1997/2/1/pubmed PY - 1997/2/1/medline PY - 1997/2/1/entrez SP - 813 EP - 22 JF - Journal of molecular and cellular cardiology JO - J. Mol. Cell. Cardiol. VL - 29 IS - 2 N2 - We recently reported that intrarenal vascular AT1 angiotensin II (ANG II) receptors are major determinants of the increased vascular resistance and reactivity to ANG II observed in the kidney of spontaneously hypertensive rats (SHR). We decided to test the hypothesis that, by modifying plasma ANG II levels by inhibiting the ANG II-converting enzyme (ACE) with captopril, we would modify intrarenal ANG II receptors, and therefore the renal vascular response to ANG II. Two approaches were taken: (1) radioligand binding assays were performed on membrane preparations of purified renal microvessels and glomeruli, with displacement of 125I-[Sar-Ile8]-ANG II by specific non-peptide antagonists of AT (losartan) and AT2 (PD 123319): (2) dose-response curves to ANG II on the isolated perfused kidney were studied. Two weeks of captopril treatment significantly reduced blood pressure (BP) and relative heart weight, and increased plasma renin activity. The binding assays showed that renal microvessels and glomeruli expressed a single receptor population (AT1) for ANG II. The density of glomerular AT1 was not modulated by captopril treatment (600 +/- 174 v 573 +/- 97 fmol/mg protein in non-treated and treated SHR respectively); however. AT1 density on the intrarenal arteries increased 3-fold (55 +/- 20 v 154 +/- 30 fmol/mg protein in non-treated and treated SHR respectively. P < 0.05). Experiments with isolated perfused kidneys demonstrated that captopril did not improve the compliance of intrarenal vessels to high flow but increased their reactivity to ANG II (ED50 = 18 nM v 0.5 pM, P < 0.01). We conclude that treatment with an ACE inhibitor increases vascular reactivity to ANG II which may be mediated by an upregulation of renal vascular ANG II receptors. SN - 0022-2828 UR - https://www.unboundmedicine.com/medline/citation/9140837/Effect_of_angiotensin_converting_enzyme_two_week_inhibition_on_renal_angiotensin_II_receptors_and_renal_vascular_reactivity_in_SHR_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(96)90304-1 DB - PRIME DP - Unbound Medicine ER -