Nifedipine‐sensitive noradrenergic vasoconstriction is enhanced in spontaneously hypertensive rats: the influence of chronic captopril treatment

Abstract

The contribution of nifedipine-sensitive component to noradrenergic vasoconstriction is enhanced during excessive NE stimulation (increased sympathetic tone of SHR in vivo or supramaximal NE stimulation in vitro). It seems that captopril-induced reduction of central sympathetic tone is able to normalize augmented nifedipine-sensitive vasoconstriction in SHR.

Vasodilator efficiency of endogenous prostanoids, Ca2+-activated K+ channels and nitric oxide in rats with spontaneous, salt-dependent or NO-deficient hypertension

“…Nelson et al 40 described the activation of L-VDCCs after norepinephrine stimulation, which results in an enhanced Ca 2+ influx. Our earlier study 4 demonstrated that a Ca 2+ influx through L-VDCCs during the tonic phase of norepinephrineinduced vascular contraction represents a decisive part of enhanced sympathetic vasoconstriction in SHRs. Moreover, Kuneš et al 5 reported an increased nifedipine-sensitive BP component in all three forms of experimental hypertension examined in the present study.…”

“…3,4 All these forms of experimental hypertension are characterized by sympathetic hyperactivity leading to an enhanced Ca 2+ influx through L-type voltage-dependent Ca 2+ channels (L-VDCCs), which is reflected by an enhanced BP response to the acute administration of Ca 2+ channel blockers, such as nifedipine. 4,5 Much less attention has been paid to vasodilator systems (except for NO) in various forms of experimental hypertension.…”

“…3,4 All these forms of experimental hypertension are characterized by sympathetic hyperactivity leading to an enhanced Ca 2+ influx through L-type voltage-dependent Ca 2+ channels (L-VDCCs), which is reflected by an enhanced BP response to the acute administration of Ca 2+ channel blockers, such as nifedipine. 4,5 Much less attention has been paid to vasodilator systems (except for NO) in various forms of experimental hypertension. It seems that the magnitude of the BP response to acute inhibition of NO synthase by N G -nitro-L-arginine methyl ester (L-NAME) injection is preserved in both salt and spontaneous hypertension, 1,4 but NO-dependent vasodilatation is clearly insufficient in compensating for major sympathetic hyperactivity, indicating a relative NO deficiency in rats with these forms of hypertension.…”

“…4,5 Much less attention has been paid to vasodilator systems (except for NO) in various forms of experimental hypertension. It seems that the magnitude of the BP response to acute inhibition of NO synthase by N G -nitro-L-arginine methyl ester (L-NAME) injection is preserved in both salt and spontaneous hypertension, 1,4 but NO-dependent vasodilatation is clearly insufficient in compensating for major sympathetic hyperactivity, indicating a relative NO deficiency in rats with these forms of hypertension. 6,7 The synthesis and/or release of vasodilator prostanoids (namely prostacyclin (PGI 2 )) has been found to be increased in the blood vessels of Dahl salt-hypertensive (DS-HS) rats, 8,9 DOCA-salt hypertensive rats and spontaneously hypertensive rats (SHRs), 10,11 but not in prehypertensive SHRs.…”

Ontogenetic changes in contribution of calcium sensitization and calcium entry to blood pressure maintenance of Wistar–Kyoto and spontaneously hypertensive rats

“…The role of enhanced calcium entry through L-type voltagedependent calcium channels (L-VDCCs) in genetic hypertension is well known [6][7][8][9], but less attention has been paid to the changes of calcium sensitization (mediated by RhoA/Rho kinase pathway) in spontaneously hypertensive rats (SHRs) [10][11][12]. Recently, we have demonstrated that basal calcium sensitization [determined in animals subjected to a blockade of major pressor systems -sympathetic nervous system (SNS) and renin-angiotensin system (RAS)] is decreased in adult SHR compared with Wistar-Kyoto (WKY) controls [13].…”