1999
DOI: 10.1006/jmcc.1998.0844
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Endothelial Dysfunction: From Physiology to Therapy

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Cited by 426 publications
(299 citation statements)
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“…Interestingly, dysfunctional endothelium-dependent vasodilator responses have been demonstrated in the vasculature of various hypertensive animal models. 2 However, endothelial abnormalities associated with hypertension may not fully explain the mechanism for the decreased erectile response in hypertensive rat models. A large part of nitric oxide release during erection is thought to be generated by neuronal nitric oxide synthase (nNOS) through the stimulation of the nonadrenergic, noncholinergic nerves to the corpus cavernosum.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Interestingly, dysfunctional endothelium-dependent vasodilator responses have been demonstrated in the vasculature of various hypertensive animal models. 2 However, endothelial abnormalities associated with hypertension may not fully explain the mechanism for the decreased erectile response in hypertensive rat models. A large part of nitric oxide release during erection is thought to be generated by neuronal nitric oxide synthase (nNOS) through the stimulation of the nonadrenergic, noncholinergic nerves to the corpus cavernosum.…”
Section: Discussionmentioning
confidence: 99%
“…[1][2][3] The pathological changes resulting from altered vascular functioning include injury to the brain, kidney and heart. Various studies have established a clinical correlation between incidence of hypertension and erectile dysfunction.…”
Section: Introductionmentioning
confidence: 99%
“…The endothelium regulates the contractility of the underlying vascular smooth muscle cells by releasing a number of factors, the most important of which are the nitric oxide (NO) and endothelium derived hyperpolarizing factor (EDHF). These two factors play a major role in the controlling of vascular homeostasis [4649]. Endothelial NO-release is related to an activation of the endothelial nitric oxide synthase (eNOS) and can be stimulated by various agonists.…”
Section: Cardiovascular Effectmentioning
confidence: 99%
“…Angiotensin II could be partly responsible for endothelial dysfunction because it induces resistance to the vasodilatory effect of the NO, so that by stopping the production of angiotensin II the direct and indirect vasoconstrictive effects of this peptide are blocked. 9 Another possible contribution of DM to endothelial dysfunction is the impairment of the lipid profile; it has been demonstrated that hypercholesterolaemia accelerates the deficit of intracellular arginine, reducing the activity of the NO synthetase, lowering the production of NO and increasing endothelin secretion predominating the vasoconstrictive response. It is important to remark that the development of the atherosclerotic process begins with an initial injury produced either by a metabolic trauma like diabetes, hypercholesterolaemia, smoking, infections, ischaemia, etc; or by a physical trauma such as hypertension and percutaneous coronary angioplasty.…”
Section: Journal Of Human Hypertensionmentioning
confidence: 99%