Alteration of extracellular calcium dependence in vascular tissue by reserpine

Garrett, R.L.; Carrier, Oliver

doi:10.1016/0014-2999(71)90219-6

Cited by 21 publications

(8 citation statements)

References 8 publications

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“…These data, in conjunction with the decrease in the rate of tension decline, and the apparent increase in the size of the slow-clearing component of 4SCa2+ loss, indicate that the tissue has an increased exchangeable fraction and, in addition, has a greater ability to retain and maintain the calcium stores involved in contraction. Previous studies (Hudgins & Harris, 1970;Garrett & Carrier, 1971; have shown that reserpine-induced supersensitivity is associated with an increased ability of the tissue to bind calcium. This may explain the increase in maximum tension seen in these studies.…”

Section: Methodsmentioning

confidence: 99%

“…Carrier & Shibata (1967) proposed that reserpine-treatment induced changes in essential ions (Na+, K+, and Ca2+) leading to an increased cellular excitability and consequential supersensitivity. Many authors (Carrier & Shibata, 1967;Hudgins, 1969;Hudgins & Harris, 1970;Garrett & Carrier, 1971; have been proponents of the involvement of the calcium ion in reserpine-induced supersensitivity. Fleming (1972) has demonstrated a partial depolarization of cell membranes of the vas deferens following treatment of guinea-pigs with reserpine and suggests it plays a role in supersensitivity.…”

Section: Methodsmentioning

confidence: 99%

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The Relationship Between Calcium and Increased Sensitivity of Rabbit Aortae Four Hours After Reserpine

Carrier

Hester

1976

British J Pharmacology

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Four hours after reserpine, rabbit aortic strips were supersensitive to acetylcholine, isoprenaline and noradrenaline. The threshold concentration of the drugs necessary to induce a response was less and the maximum tension developed by the tissues was greater than in control strips. Reserpine‐treatment potentiated the contractile responses to CaCl2. Reserpine‐treatment resulted in an increase in calcium uptake and an increase in the slow component of 45Ca2+ efflux. After resperine‐treatment, the rate of relaxation from a potassium‐induced contraction was decreased. It is concluded that reserpine‐induced supersensitivity is related to an enhanced ability of the tissue to retain and utilize calcium.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

The Relationship Between Calcium and Increased Sensitivity of Rabbit Aortae Four Hours After Reserpine

Carrier

Hester

1976

British J Pharmacology

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“…This suggestion is similar to the theory of rcserpinc-induced supersensi tivity of vascular smooth muscle, i.e.. that the resulting increase in maximum contrac tile responses to norepinephrine, KCI and other agonists arc at least in part due to an increased availability of intracellular calcium [Carrier and Jure vies. 1973;Carrier and Hes ter, 1976;Garrett and Carrier, 1971], Al though supersensitivity is usually character ized by a decrease in the EC50 value for an agonist, the increase in maximum contractile force described in the present study may be a manifestation of a nonspecific type of ago nist-induced supersensitivity.…”

Section: Discussionmentioning

confidence: 91%

Effects of Repetitive Stimulation by Norepinephrine, Histamine or Potassium Chloride on Contractile Responses of Pulmonary Vascular Smooth Muscle

Howell¹,

Carrier²

1986

Pharmacology

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We examined consecutive contractile responses of isolated rabbit pulmonary arteries during repeated exposures to either norepinephrine, histamine or KCl, with washout and relaxation between trials. For each agonist, EC₅₀ values remained constant during consecutive determinations, but the maximum force increased after the first determination. A maximum concentration of norepinephrine or histamine produced a biphasic contraction: the fast phase increased subsequent to the first determination and was retained in a calcium-free medium, while the slow phase was unaltered during consecutive determinations and was absent in a calcium-free medium. We conclude that in the rabbit pulmonary artery: (l)the initial contractile response is a useful control for studies of sensitivity but not of maximum activity; (2) there may be a nonspecific increase in the availability of intracellular calcium after the initial contraction and relaxation, and (3) desensitization or tachyphylaxis to these agonists does not occur.

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“…The case for potassium is more com plicated. Potassium-induced contractions of poorly innervated vascular smooth muscles, such as aorta, are independent of noradrena line release [Shibata and Carrier, 1967], Such contractions are not inhibited by aadrenoreceptor blocking agents such as phentolamine (10~4 A/) or by reserpine [Garret and Carrier, 1971], In the densely innervated rat tail artery, phentolamine (1 O'6 or 10-5 M) inhibits 35-50% of the vasocon striction induced by potassium [Webb et al, 1978[Webb et al, , 1983. We found that phentol amine (4 X 10~b M ) blocks potassium-in duced vasoconstriction (40 mM) by 95% [unpubl.…”

Section: Discussionmentioning

confidence: 99%

Changes in the Vascular Reactivity of the Isolated Tail Arteries of Spontaneous and Renovascular Hypertensive Rats to Endogenous and Exogenous Noradrenaline

et al. 1987

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We have investigated the changes in the responses to noradrenaline of isolated tail arteries of spontaneously hypertensive (SHR) and renovascular hypertensive rats (Wistar-Kyoto: two-kidney, one-clip model, WKY:2K1C) compared with normotensive (Wistar-Kyoto, WKY) rats. Renovascular hypertension was induced by 4 weeks’ unilateral renal artery clipping. Arteries were vasoconstricted with exogenous noradrenaline, electrical field stimulation or high potassium. The effects of the latter two stimuli were abolished by reserpine and so were presumably dependent on the presence of endogenous noradrenaline. In the SHR the maximal vasoconstriction produced by all three stimuli was greater than in WKY. Dose-response curves were steeper and there was no change in threshold. Vascular mass was greater. We interpret these results as showing an increase in vascular reactivity in the SHR caused by structural adaptation. The WKY:2K1C responses to noradrenaline could also be explained in terms of structural adaptation but there was no increase in vascular mass. Sensitivity to potassium and electrical stimulation was decreased, suggesting a defect in vascular neurotransmission. This was supported by the observations of a decreased arterial noradrenaline content and of decreased sensitivity to cocaine.

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Alteration of extracellular calcium dependence in vascular tissue by reserpine

Cited by 21 publications

References 8 publications

The Relationship Between Calcium and Increased Sensitivity of Rabbit Aortae Four Hours After Reserpine

The Relationship Between Calcium and Increased Sensitivity of Rabbit Aortae Four Hours After Reserpine

Effects of Repetitive Stimulation by Norepinephrine, Histamine or Potassium Chloride on Contractile Responses of Pulmonary Vascular Smooth Muscle

Changes in the Vascular Reactivity of the Isolated Tail Arteries of Spontaneous and Renovascular Hypertensive Rats to Endogenous and Exogenous Noradrenaline

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