Systemic and renal effects of a new angiotensin converting enzyme inhibitor, benazepril, in essential hypertension

Valvo, E.; Casagrande, P; Bedogna, Valeria; Antiga, Leopoldo; Alberti, Daniele; Zamboni, M.; Perobelli, L.; Santo, Francesca Dal; Maschio, G

doi:10.1097/00004872-199011000-00003

Cited by 14 publications

(4 citation statements)

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“…These whole kidney hemodynamic responses to blockade of the RAS have frequently been interpreted as indicating that ACE inhibitors and AT 1 receptor blockers predominantly dilate the efferent arterioles [1092,[1174][1175][1176][1177][1178] . These whole kidney hemodynamic responses to blockade of the RAS have frequently been interpreted as indicating that ACE inhibitors and AT 1 receptor blockers predominantly dilate the efferent arterioles [1092,[1174][1175][1176][1177][1178] .…”

Section: Responses To Ace Inhibitors and Ang II Receptor Blockersmentioning

confidence: 99%

The Renal Microcirculation

et al. 2008

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Section: Responses To Ace Inhibitors and Ang II Receptor Blockersmentioning

confidence: 99%

The Renal Microcirculation

et al. 2008

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“…These results are also consistent with earlier studies on ACE-inhibitors. 27,28 Moreover, in the study by Chiolero et al 10 the plasma renin activity and serum aldosterone levels showed no differences in the respective tertiles of sodium sensitivity of hypertension (when consuming either low sodium diet or-and particularly-high sodium diet). Thus, these results may indicate that the inter-tertile differences of FE Li were completely independent of the renin-angiotensin-aldosterone activity.…”

Section: Discussionmentioning

confidence: 90%

Blood pressure and arterial stiffness in patients with high sodium intake in relation to sodium handling and left ventricular diastolic dysfunction status

et al. 2015

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In a population with high sodium consumption, we assessed relation between brachial and central blood pressures, elastic properties of large arteries, echocardiographic left ventricular diastolic function and sodium reabsorption as fractional urinary lithium excretion in proximal (FELi) and fractional sodium reabsorption in distal tubules assessed using the endogenous lithium clearance. Mean±s.d. age of 131 treated hypertensive patients (66 men and 65 women) was 61.9±7.5 years. We found significant interaction between left ventricular diastolic function and FELi with respect to the values of brachial blood pressure: systolic (SBP), diastolic (DBP) and mean blood pressure (MBP) (all PINT<0.03). In patients with FELi below the median value and impaired left ventricular diastolic function, the values of SBP (149.3 vs 132.5 mm Hg; P=0.005), DBP (85.1 vs 76.1 mm Hg; P=0.001), MBP (106.5 vs 94.9 mm Hg; P=0.001), central SBP (SBPC) (137.4 vs 122.0 mm Hg; P=0.01), central DBP (DBPC) (84.8 vs 76.0 mm Hg; P=0.003), central MBP (MBPC) (106.9 vs 95.9 mm Hg; P=0.007), aortic pulse wave augmentation (18.0 vs 13.5 mm Hg; P=0.03), pulse wave velocity (14.6 vs 12.5 m s(-1); P=0.02) and central aortic pulse wave augmentation index (155.7% vs 140.9%; P=0.01) were significantly higher than in patients with normal left ventricular diastolic function. Such relationships were not observed in the entire group and patients with FELi above the median value. In the hypertensive population with high sodium intake, increased sodium reabsorption in proximal tubules may affect blood pressure parameters and arterial wall damage, thus contributing to the development of left ventricular diastolic function impairment.

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“…Benazepril, also known as Lotensin, is an ACEI that was approved by the US Food and Drug Administration in 1991. There are numerous pharmacodynamic data regarding benazepril (70)(71)(72). According to an extensive review regarding the pharmacodynamic and pharmacokinetic properties of benazepril (73), benazepril remarkably suppresses human plasma and tissue Ang II levels via inhibiting ACE activity by ~80-90% both in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

TRPM8 downregulation by angiotensin II in vascular smooth muscle cells is involved in hypertension

Huang

Zhang

et al. 2017

Molecular Medicine Reports

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Angiotensin II (Ang II)-induced injury of vascular smooth muscle cells (VSMCs) serves an important role in hypertension and other cardiovascular disorders. Transient receptor potential melastatin 8 (TRPM8) is a thermally‑regulated Ca2+‑permeable channel that is activated by reduced body temperature. Although several recent studies have revealed the regulatory effect of TRPM8 in vascular tone and hypertension, the precise role of TRPM8 in dysfunction of vascular smooth muscle cells (VSMCs) induced by Ang II remains elusive. In the present study, the possible function of TRPM8 in Ang II‑induced VSMCs malfunction in vivo and in vitro was investigated. In the aortae from rats that had undergone a two‑kidney one‑clip operation, which is a widely‑used renovascular hypertension model, the mRNA and protein levels of TRPM8 were reduced. In addition, exogenous Ang II treatment decreased TRPM8 mRNA and protein expression levels in primary cultures of rat VSMCs. TRPM8 activation by menthol, a pharmacological agonist, in VSMCs, significantly attenuated the Ang II‑induced increase in reactive oxygen species and H2O2 production. In addition, TRPM8 activation reduced the Ang II‑induced upregulation of NADPH oxidase (NOX) 1 and NOX4 in VSMCs. Furthermore, TRPM8 activation relieved the Ang II‑induced activation of ras homolog gene family, member A‑rho associated protein kinase 2 and janus kinase 2 signaling pathways in VSMCs. In conclusion, the results presented in the current study indicated that TRPM8 downregulation by Ang II in VSMCs may be involved in hypertension.

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Systemic and renal effects of a new angiotensin converting enzyme inhibitor, benazepril, in essential hypertension

Cited by 14 publications

References 0 publications

The Renal Microcirculation

The Renal Microcirculation

Blood pressure and arterial stiffness in patients with high sodium intake in relation to sodium handling and left ventricular diastolic dysfunction status

TRPM8 downregulation by angiotensin II in vascular smooth muscle cells is involved in hypertension

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