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Circulation. 2000 Apr 18;101(15):1854-60.
Impaired endothelium-dependent regulation of ventricular relaxation in pressure-overload cardiac hypertrophy.

MacCarthy PA, Shah AM.

Department of Cardiology, University of Wales College of Medicine, Cardiff, UK.

BACKGROUND: Endothelium-derived nitric oxide (NO) selectively enhances myocardial relaxation and may benefit diastolic function. Left ventricular hypertrophy (LVH) is characterized by abnormal myocardial relaxation and endothelial dysfunction. We investigated endothelium-dependent regulation of LV relaxation in moderate pressure-overload LVH induced by aortic banding in guinea pigs. METHODS AND RESULTS: Isolated ejecting hearts of banded or sham-operated animals (shams) were studied. The specific agonists for endothelial release of NO, bradykinin (10 nmol/L), and substance P (100 nmol/L) both induced earlier onset of LV relaxation in shams (time to LV dP/dt(min) [tdP/dt(min)], -13.4+/-3.0 and -10.4+/-2.5 ms, respectively) without altering peak LV pressure or LV dP/dt(max). Neither agent altered tdP/dt(min) in banded animals. The ACE inhibitor captopril (1 micromol/L) also selectively reduced tdP/dt(min) in shams via a bradykinin/NO-dependent mechanism but had no effect in banded animals. An exogenous NO donor, sodium nitroprusside (0.1 micromol/L), selectively reduced tdP/dt(min) to a similar extent in both shams and banded animals. Endothelial-type NO synthase (eNOS) protein expression in whole LV homogenate was unaltered in banded animals. CONCLUSIONS: Endothelium-dependent enhancement of LV relaxation is impaired in moderate pressure-overload LVH, despite a preserved response to exogenous NO. This is not accounted for by altered eNOS expression. These abnormalities may contribute to diastolic dysfunction in LVH.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10769288&dopt=Abstract

Horm Behav. 1991 Dec;25(4):461-76.
Blood-borne and cerebral angiotensin and the genesis of salt intake.

Yang ZF, Epstein AN.

Department of Biology, University of Pennsylvania.

These experiments reevaluate earlier work in which salt intake was evoked by blood-borne angiotensin II. That work is inconsistent with recent demonstrations that cerebral, not blood-borne, angiotensin II is the synergist with aldosterone in arousing salt intake in the rat. We show, first, that the pharmacological doses of angiotensin II that were used in the earlier work are natriuretic (and dipsogenic). They cause urinary sodium losses that precede and exceed sodium intake. Second, we show that the excess sodium intake that is associated with pharmacological doses of intravenous angiotensin is not caused by endogenous aldosterone. Last, we show that this excess sodium intake is abolished by intracerebroventricular captopril thereby suggesting that it is caused by activation of cerebral angiotensin II and harmonizing its mechanism with current concepts.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1813374&dopt=Abstract

Eur J Pharmacol. 2000 Apr 14;394(2-3):301-9.
Angiotensin I-converting enzyme activity and vascular sensitivity to angiotensin I in rat injured carotid artery.

Lemay J, Hou Y, Tremblay J, deBlois D.

Department of Pharmacology, Laboratory of Pharmacology of Vascular Pathologies, Centre de Recherche du C.H.U.M., Universite de Montreal, 3840 St. Urbain Street., 7-133B, Montreal, Quebec, Canada.

We used a vasoreactivity assay to examine the functional significance of angiotensin I-converting enzyme overexpression in smooth muscle cells after vascular injury. Rat carotid arteries isolated at days 2 to 14 after in vivo endothelial denudation were compared with the contralateral freshly denuded (control) vessels. Arterial rings were constricted ex vivo with angiotensin I in the absence or presence of the angiotensin I-converting enzyme inhibitors captopril (300 nM and 3 microM) or perindoprilate (1 nM). Angiotensin I-converting enzyme activity was determined by cleavage of the chromogenic substrate Hip-His-Leu. Angiotensin I-converting enzyme activity in injured arteries was increased (2-fold) at day 7 only after vascular injury. Contractions to angiotensin I were unaffected after injury. Inhibition by captopril and perindoprilate of angiotensin I-induced contractions was significantly less potent in injured arteries at day 7 as compared to control vessels. Mechanical removal of neointimal smooth muscle cells normalized the inhibition by captopril in injured arteries at day 7. Captopril did not affect angiotensin II-induced contractions. Thus, upregulation of angiotensin I-converting enzyme after arterial injury confers resistance to angiotensin I-converting enzyme inhibitors.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10771296&dopt=Abstract

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