Delayed development of hypertension after short-term nitrendipine treatment.

Rizzoni, Damiano; Castellano, Maurizio; Porteri, Enzo; Bettoni, Giorgio; Muiesan, M.L.; Rosei, Enrico Agabiti

doi:10.1161/01.hyp.24.1.131

Cited by 52 publications

(31 citation statements)

References 30 publications

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“…36 Three-month treatment with lercanidipine increased the vasodilation to bradykinin but not to sodium nitroprusside in patients with essential hypertension. Such a finding is in agreement with experimental data indicating that calcium entry blockers increase endothelial function in various animal vessels 37,38 and hypertensive patients. 20 In addition, lercanidipine treatment increased the L-NMMA-induced vasoconstrictor effect and restored the ability of L-NMMA to blunt the vasodilation to bradykinin.…”

Section: Discussionsupporting

confidence: 92%

Calcium Antagonist Treatment by Lercanidipine Prevents Hyperpolarization in Essential Hypertension

et al. 2003

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Abstract-Essential hypertension is associated with impaired endothelium-dependent vasodilation caused by oxidative stress-induced nitric oxide (NO) breakdown and compensatory production of a hyperpolarizing factor. To test whether calcium antagonist treatment can restore NO availability and prevent hyperpolarization through antioxidant properties, in 15 healthy subjects and 15 patients with essential hypertension, we studied forearm blood flow (strain-gauge plethysmography) modifications induced by intrabrachial bradykinin (5, 15, 50 ng/100 mL per minute), an endothelium-dependent vasodilator, in basal conditions, during infusion of N G -monomethyl-L-arginine (L-NMMA, 100 g/100 mL per minute), an NO-synthase inhibitor, and ouabain (0.72 g/100 mL per minute), an Na ϩ -K ϩ ATPase inhibitor to prevent hyperpolarization. These infusions were repeated in the presence of the antioxidant vitamin C (8 mg/100 mL/min). The response to sodium nitroprusside was also evaluated. In controls, vasodilation to bradykinin was inhibited by L-NMMA and remained unchanged by ouabain or vitamin C. In hypertensive patients, vasodilation to bradykinin was blunted and resistant to L-NMMA but sensitive to ouabain. Vitamin C increased the response to bradykinin and restored the inhibiting effect of L-NMMA while preventing the effect of ouabain. In hypertensive patients, infusions were repeated after 3-month treatment with lercanidipine (10 to 20 mg daily). Lercanidipine decreased plasma lipoperoxides, isoprostanes, and malondialdehyde and increased plasma antioxidant capacity. Moreover, lercanidipine increased the vasodilation to bradykinin and restored the inhibiting effect of L-NMMA on bradykinin-induced vasodilation while preventing the effect of ouabain. Finally, vitamin C no longer exerted its facilitating activity. These results indicate that in essential hypertension, lercanidipine increases endothelium-dependent vasodilation by restoring NO availability and preventing hyperpolarization, an effect probably determined by antioxidant activity. Key Words: hypertension, essential Ⅲ endothelium Ⅲ nitric oxide Ⅲ endothelium-derived factors Ⅲ free radicals Ⅲ antioxidants Ⅲ calcium antagonists E ndothelium plays a primary role in the modulation of vascular tone 1 by producing and releasing relaxing substances including nitric oxide (NO) 2 and a not-yet identified hyperpolarizing factor (EDHF). 3 In the presence of several cardiovascular risk factors, endothelial cells can also produce contracting factors (EDCFs), which are mainly cyclooxygenase-dependent prostanoids (thromboxane A2 and prostaglandin H2) 4,5 or superoxide anions. 6 Essential hypertension is characterized by impaired endothelium-dependent vasodilation to specific agonists 7-9 as the result of a reduction in NO oxide availability 10,11 caused by production of oxidative stress. 12 In the presence of impaired NO availability, endothelium-dependent relaxation seems to be sustained by hyperpolarization, which probably acts as a compensatory mechanism. 13 Since endothelial dysfunct...

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Section: Discussionsupporting

confidence: 92%

Calcium Antagonist Treatment by Lercanidipine Prevents Hyperpolarization in Essential Hypertension

et al. 2003

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“…4,22 Correlation coefficients between media-tolumen ratio measured in the two arteries obtained from each biopsy was 0.79. The protocol of the study was approved by the ethics committee of our institution (Medical School of University of Brescia), and informed consent was obtained from each participant.…”

Section: Micromyographymentioning

confidence: 99%

Acromegalic Patients Show the Presence of Hypertrophic Remodeling of Subcutaneous Small Resistance Arteries

et al. 2004

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Abstract-Structural alterations of small resistance arteries in patients with essential hypertension (EH) are mostly characterized by inward eutrophic remodeling. However, we have observed the presence of hypertrophic remodeling in patients with renovascular hypertension, as well as in patients with noninsulin-dependent diabetes mellitus, suggesting a relevant effect of humoral growth factors on vascular structure. Growth hormone may stimulate in vitro proliferation of vascular smooth muscle cells. However, no data are presently available about small artery structure in acromegalic patients. Therefore, we have investigated the structure of subcutaneous small arteries in 12 normotensive (NT) subjects, in 12 EH subjects, and in 9 acromegalic patients (APs). All subjects underwent biopsy of the subcutaneous fat; then, small resistance arteries were dissected and mounted on a micromyograph. The normalized internal diameter, media thickness, media-to-lumen ratio, the media cross-sectional area together with remodeling, and growth indices were calculated. Demographic variables were similar in the three groups, except for blood pressure. The media-to-lumen ratio was significantly greater in EH and AP, compared with NT. No difference was observed between EH and AP. The media cross-sectional area was significantly greater in AP compared with EH and with NT. The calculation of remodeling and growth index suggests the presence of eutrophic remodeling in EH (growth index 0%) and of hypertrophic remodeling in AP (growth index 40%). In conclusion, our data suggest the presence of hypertrophic remodeling of subcutaneous small resistance arteries of AP, probably as a consequence of growth-stimulator properties of IGF-1. Key Words: arteries Ⅲ hypertrophy Ⅲ remodeling Ⅲ growth hormone S tructural alterations of small resistance arteries (lumen diameter: 100 to 300 m) 1 of patients with essential hypertension (EH) are mostly characterized by inward eutrophic remodeling (rearrangement of the same wall material around a narrowed lumen). 2,3 At variance, we have observed the presence of hypertrophic remodeling (vascular smooth muscle cell hypertrophy or hyperplasia) in subcutaneous small arteries of patients with renovascular hypertension. 4 Neurohumoral factors are probably involved in the genesis of vascular structural alterations, and growth factors, such as angiotensin II, seem to be able to induce smooth muscle cell hypertrophy. 5,6 Also, patients with noninsulin-dependent diabetes mellitus showed the presence of hypertrophic remodeling of subcutaneous small arteries, 7 suggesting, again, a relevant effect of humoral growth factors on vascular structure. In fact, insulin and insulin-like growth factor-1 (IGF-1) seem to be able to stimulate cardiac and vascular smooth muscle cell growth. 8 A weak but statistically significant correlation between mediato-lumen ratio of subcutaneous small arteries and levels of circulating insulin was observed in patients with diabetes mellitus. 7 It was previously demonstrated that growth hormone ...

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“…Then, the normalized internal circumference L 1 was determined from the resting wall tension-internal circumference relation and Laplace equation (L 1 is defined as 0.9ϫL 100 , where L 100 is an estimate of the internal circumference that the vessel would have had in vivo when subjected to a transmural pressure of 100 mm Hg while relaxed). 6 From L 1 , the normalized internal diameter l 1 was calculated. With the assumption that the crosssectional area remains constant when the vessel is extended to L 1 , the previously mentioned morphological parameters were also automatically calculated in a normalized condition.…”

Section: Cardiac and Vascular Remodelingmentioning

confidence: 99%

“…With the assumption that the crosssectional area remains constant when the vessel is extended to L 1 , the previously mentioned morphological parameters were also automatically calculated in a normalized condition. 6 The remodeling index was calculated in WT and KO mice according to the following formulas:…”

Section: Cardiac and Vascular Remodelingmentioning

confidence: 99%

Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice

et al. 2002

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Background-The ␣ 1 -adrenergic receptors (␣ 1 -ARs) play a key role in cardiovascular homeostasis. However, the functional role of ␣ 1 -AR subtypes in vivo is still unclear. The aim of this study was to evaluate the cardiovascular influences of ␣ 1b -AR. Methods and Results-In transgenic mice lacking ␣ 1 -AR (KO) and their wild-type controls (WT), we evaluated blood pressure profile and cardiovascular remodeling induced by the chronic administration (18 days via osmotic pumps) of norepinephrine, angiotensin II, and subpressor doses of phenylephrine. Our results indicate that norepinephrine induced an increase in blood pressure levels only in WT mice. In contrast, the hypertensive state induced by angiotensin II was comparable between WT and KO mice. Phenylephrine did not modify blood pressure levels in either WT or KO mice. The cardiac hypertrophy and eutrophic vascular remodeling evoked by norepinephrine was observed only in WT mice, and this effect was independent of the hypertensive state because it was similar to that observed during subpressor phenylephrine infusion. Finally, the cardiac hypertrophy induced by thoracic aortic constriction was comparable between WT and KO mice. Conclusions-Our data demonstrate that the lack of ␣ 1b -AR protects from the chronic increase of arterial blood pressure induced by norepinephrine and concomitantly prevents cardiovascular remodeling evoked by adrenergic activation independently of blood pressure levels. (Circulation. 2002;105:1700-1707.)

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Delayed development of hypertension after short-term nitrendipine treatment.

Cited by 52 publications

References 30 publications

Calcium Antagonist Treatment by Lercanidipine Prevents Hyperpolarization in Essential Hypertension

Calcium Antagonist Treatment by Lercanidipine Prevents Hyperpolarization in Essential Hypertension

Acromegalic Patients Show the Presence of Hypertrophic Remodeling of Subcutaneous Small Resistance Arteries

Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice

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Delayed development of hypertension after short-term nitrendipine treatment.

Cited by 52 publications

References 30 publications

Calcium Antagonist Treatment by Lercanidipine Prevents Hyperpolarization in Essential Hypertension

Calcium Antagonist Treatment by Lercanidipine Prevents Hyperpolarization in Essential Hypertension

Acromegalic Patients Show the Presence of Hypertrophic Remodeling of Subcutaneous Small Resistance Arteries

Cardiovascular Influences of α 1b -Adrenergic Receptor Defect in Mice

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Product

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Cardiovascular Influences of α _1b -Adrenergic Receptor Defect in Mice