Structure and function of resistance arteries of hypertensive patients treated with a p-blocker or a calcium channel antagonist

Schiffrin, Ernesto L.; Deng, Li

doi:10.1097/00004872-199610000-00014

Cited by 176 publications

(117 citation statements)

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“…In fact, a linear relation between M/L of subcutaneous small resistance arteries and left ventricular mass index or relative wall thickness has been detected in hypertensive patients; this relation with left ventricular mass and geometry was more evident in patients with activation of the renin-angiotensinaldosterone system. 26 It is interesting to note that several studies have demonstrated that the effect of different antihypertensive drugs on vascular structure is not the same, being clearly more effective for those drugs that interfere with the renin-angiotensin system [27][28][29] and calcium antagonists 30 than for ␤-blockers.…”

Section: Rizzoni Et Al Prognostic Role Of Small-artery Structurementioning

confidence: 99%

Prognostic Significance of Small-Artery Structure in Hypertension

et al. 2003

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Background-The presence of structural alterations in the microcirculation may be considered an important mechanism of organ damage; however, it is not currently known whether structural alterations of small arteries may predict fatal and nonfatal cardiovascular events. Methods and Results-One hundred twenty-eight patients were included in the present study. There were 59 patients with essential hypertension, 17 with pheochromocytoma, 20 with primary aldosteronism, 12 with renovascular hypertension, and 20 normotensive patients with non-insulin-dependent diabetes mellitus. All subjects were submitted to a biopsy of subcutaneous fat. Small resistance arteries were dissected and mounted on an isometric myograph, and the tunica media-to-internal lumen ratio (M/L) was measured. The subjects were reevaluated after an average follow-up time of 5.4 years. Thirty-seven subjects had a documented fatal or nonfatal cardiovascular event (5.32 events/100 patients per year). In the subcutaneous small arteries of subjects with cardiovascular events, a smaller internal diameter and a clearly greater M/L was observed. Our subjects were subdivided according to the presence of an M/L greater or smaller than the mean and median values observed in the whole population (0.098) or mean value ϩ2 SD of our normal subjects (0.11). Life-

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Section: Rizzoni Et Al Prognostic Role Of Small-artery Structurementioning

confidence: 99%

Prognostic Significance of Small-Artery Structure in Hypertension

et al. 2003

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“…[43][44][45][46][47][48][49][50][51][52][53]210 However, depending on the antihypertensive drug and its pharmacological profile, improvements in endothelium-dependent vasodilation can be achieved (Table 1). 45,47,49,[211][212][213][214][215][216][217][218][219][220][221] The multifactorial aetiology of essential hypertension as well as the duration of blood pressure elevation may explain certain inconsistent results of different investigators. 222,223 Besides certain ACE-inhibitors, several calcium channel blocking agents were successful in improving endothelial function in human hypertension (Table 1).…”

Section: Effects Of Antihypertensive Therapy On Endothelial Function mentioning

confidence: 99%

Working under pressure: the vascular endothelium in arterial hypertension

et al. 2000

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The vascular endothelium synthesizes and releases a spectrum of vasoactive substances like nitric oxide (NO) and endothelin (ET). In hypertension, the delicate balance of endothelium-derived factors is disturbed. ET acts as the natural counterpart to endothelium-derived NO, which exerts vasodilating, antithrombotic, and antiproliferative effects, and inhibits leukocyte-adhesion to the vascular wall. Besides its blood pressure rising effect also in man, ET induces vascular and myocardial hypertrophy, which are independent risk factors for cardiovascular morbidity and mortality. The derangement of endothelial function in hypertension is likely to be caused in part by genetic factors, but also due to elevated blood pressure itself. Due to its position between blood pressure and smooth muscle cells responsible for peripheral resistance, the endothelium is thought to be both target and mediator of arterial hypertension. Oxi-

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“…19,22,30 Studies in humans have given less consistent results, 39,[42][43][44][45][46] but some found improvement in endothelial function after shortor long-term drug treatments. 39,42,46,47 ACh-induced relaxation in the rat mesenteric artery is determined by the balance of NO, EDHF, and endotheliumderived contracting factor. 10,26,48 The present study demonstrated that 3 months of antihypertensive treatment in SHRs improved endothelium-dependent relaxation in response to ACh in mesenteric arteries precontracted with NE.…”

Section: Effects Of Antihypertensive Treatments On Edhf-mediated Relamentioning

confidence: 99%

“…59 In addition, several studies revealed that part of the endothelium-dependent relaxation to various agonists in isolated human blood vessels (such as coronary, 58 omental, 60 and cerebral 59 arteries) is resistant to a combined blockade of cyclooxygenase and NO synthase but is eventually abolished by a high-K ϩ solution, suggesting a possible role of EDHF in the relaxation. It remains to be seen whether alteration in the EDHF-mediated response is involved in endothelial dysfunction in hypertension [43][44][45] and its improvement by drug therapy 39,42,46,47 in humans.…”

Section: Clinical Relevancementioning

confidence: 99%

Antihypertensive Treatment Improves Endothelium-Dependent Hyperpolarization in the Mesenteric Artery of Spontaneously Hypertensive Rats

et al. 1998

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Background-The vascular endothelium releases endothelium-derived hyperpolarizing factor (EDHF). The mesenteric arteries of 6-to 8-month-old spontaneously hypertensive rats (SHRs) exhibit an impairment of the hyperpolarization induced by acetylcholine via EDHF. Methods and Results-We determined whether antihypertensive treatment can improve EDHF-mediated responses inSHRs. Beginning at age 8 to 9 months, the animals were treated with either enalapril (40 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 ) (SHR-Es) or a combination of hydralazine (25 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 ) and hydrochlorothiazide (7.5 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 ) (SHR-Hs) for 3 months. The control groups were age-matched SHRs (SHR-Cs) and Wistar Kyoto rats (WKYs). The two treatments lowered the blood pressure to comparable extents. The acetylcholine-induced hyperpolarization in the mesenteric artery of treated SHRs improved to a level comparable to that in WKYs (acetylcholine 10 Ϫ5 mol/L with norepinephrine 10

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Structure and function of resistance arteries of hypertensive patients treated with a p-blocker or a calcium channel antagonist

Cited by 176 publications

References 0 publications

Prognostic Significance of Small-Artery Structure in Hypertension

Prognostic Significance of Small-Artery Structure in Hypertension

Working under pressure: the vascular endothelium in arterial hypertension

Antihypertensive Treatment Improves Endothelium-Dependent Hyperpolarization in the Mesenteric Artery of Spontaneously Hypertensive Rats

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