Hyperosmolarity: effects on nerves and smooth muscle of cutaneous veins

McGrath, MA; Shepherd, JT

doi:10.1152/ajplegacy.1976.231.1.141

Cited by 34 publications

(15 citation statements)

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“…Probably the hormone-modulated contraction of endothelial cells in such vessels, with increase in vascular permeability and exudation of macromolecules, is a major event. As pointed out by Vanhoutte (1978), changes in composition of extracellular fluid, if only from the osmotic point of view, may provide an acceptable basis for vasodilatation, because hyperosmolarity inhibits vascular smooth muscle reactivity (Mellander & Lundvall, 1971;Haddy & Scott, 1975;McGrath & Shepherd, 1976). Accordingly, histamine and bradykinin might antagonize the vasoconstrictor response to noradrenaline through an increase in vascular permeability, from which osmotic changes of the extracellular fluid resulted.…”

Section: Discussionmentioning

confidence: 99%

Influence of diabetes on the reactivity of mesenteric microvessels to histamine, bradykinin and acetylcholine

Fortes

Leme

Scivoletto

1983

British J Pharmacology

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1 Noradrenaline (NA) evoked a vasoconstrictor response in rat mesenteric microvessels in situ, the latency and nature of which was analogous in normal and alloxan-diabetic animals. 2 Histamine and bradykinin (Bk) were capable of antagonizing the response to NA in normal but not in diabetic animals. In contrast, acetylcholine (ACh) was equally effective as an antagonist to NA in both groups of animals. 3 The altered responses to histamine and Bk were not associated with hyperglycaemia since fasting rendered the diabetic animals normoglycaemic and yet did not restore the reactivity of microvessels. Previous administration of insulin to diabetic animals corrected the impaired responses to histamine and Bk.4 A similar condition of impaired responses to histamine and Bk was produced in normal animals by the intravenous injection of 2-deoxyglucose although ACh remained fully active. 5 Apparently, the functional changes observed in the response to histamine or Bk, as antagonists of the vasoconstrictor reaction to NA, were not associated with a defective response of all smooth muscle. First, because ACh remained active in diabetic animals, and, second, because extravascular smooth muscles obtained from either normal or diabetic rats were equally relaxed by histamine or Bk in vitro.6 It is suggested that histamine and Bk antagonized the vasoconstrictor response of microvessels to NA through an action on lining endothelial cells resulting in increased vascular permeability and hyperosmolarity of extracellular fluids. 7 The process depended on the availability of insulin, and, therefore, might be affected by intracellular glucopaenia as occurring in diabetes. 8 Intracellular glucopaenia markedly affected other structures. Reduced atria rates were observed in diabetes, despite the fact that the isolated preparation responded normally to NA, ACh or tyramine. Partial substitution of glucose in the bathing fluid by 2-deoxyglucose or addition of NaF to the organ bath evoked similar changes in atria from normal animals.9 ACh which has little effect on vascular permeability must exert its vasodilator effects through mechanisms which are different from those influenced by the biochemical changes occurring in diabetes.

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Section: Discussionmentioning

confidence: 99%

Influence of diabetes on the reactivity of mesenteric microvessels to histamine, bradykinin and acetylcholine

Fortes

Leme

Scivoletto

1983

British J Pharmacology

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“…Depression of the excitation induced by noradrenaline on helical strips from veins is observed on increasing the osmolarity of the bathing fluid (McGrath & Shepherd, 1976). Furthermore, in microvessel beds of the cheek pouch and cremaster muscle of the hamster, arteriolar dilatation is produced by suffusing the tissues with hyperosmotic solutions.…”

Section: Discussionmentioning

confidence: 99%

Vascular reactivity in diabetes mellitus: role of the endothelial cell

Fortes

Lerne

Scivoletto

1983

British J Pharmacology

130

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1 The response to vasoactive agents of microvessels in situ and large arteries in vitro was compared in normal and alloxan-diabetic rats. 2 Noradrenaline was equally effective in evoking a constrictor response of mesenteric microvessels in normal and diabetic animals. 3 The constrictor response to a standard amount of noradrenaline in such vessels was fully antagonized by acetylcholine or papaverine, the minimum effective doses being equivalent in normal and diabetic animals. In contrast, the minimum doses of histamine or bradykinin, effective in normal animals, had to be increased about 20 fold to be active in diabetic animals. 4 Increased osmolarity of extracellular fluid caused a significant and equivalent increase in latency of the vasoconstrictor response of microvessels to noradrenaline in normal and diabetic animals. 5 Concentration-effect curves, constructed from the response of isolated aortae to noradrenaline, were similar in normal and diabetic animals, provided the endothelium was removed. Diabetes only affected preparations in which the endothelium was left intact. In these, the median effective concentrations of noradrenaline were greatly increased in comparison with normal values. 6 Precontracted aortae from normal and diabetic animals were equally relaxed by acetylcholine and histamine, provided the endothelium was left intact. Loss of the relaxant response of the preparations in all groups of animals was observed following removal of endothelial cells. 7 It is suggested that different mechanisms may be involved in the effects of vasodilator agents on large arteries in vitro or small vessels in situ. Histamine and bradykinin which are potent permeability-increasing factors, may antagonize the vasoconstrictor response of microvessels to noradrenaline through an action on endothelial cells with increased vascular permeability and temporary changes in composition of extracellular fluid. The reactive process of endothelial cells to permeability factors was affected by diabetes mellitus. However, the response of microvessels to acetylcholine and papaverine which are devoid of permeability-increasing properties, was not influenced by diabetes.

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“…There have been few studies reporting the effects of hypertonic solutions on vascular smooth muscle in exper imental animals [14][15][16][17][18]. Contractile responses to hyper tonic solutions have been demonstrated in dog aorta [14], dog saphenous vein [15], dog terminal mesenteric arteries [16], rabbit aorta [17], and rat aorta [18].…”

Section: Discussionmentioning

confidence: 99%

“…Contractile responses to hyper tonic solutions have been demonstrated in dog aorta [14], dog saphenous vein [15], dog terminal mesenteric arteries [16], rabbit aorta [17], and rat aorta [18]. To our knowl edge, there have been no studies on human vascular smooth muscle.…”

Section: Discussionmentioning

confidence: 99%

Contractile Responses in Human Umbilical Arteries to Hyper- and Hypotonic Solutions

Sato

Kojima²,

Dohi³

1994

J Vasc Res

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The effects of hyper- and hypotonic solutions on vascular smooth muscle were studied using helical strips from human umbilical arteries. Hypertonic solutions evoked a biphasic contraction that consisted of early and late contractions. Verapamil or Ca²⁺-free conditions inhibited early contraction induced by tonicity of 340-539 mosm/kg. Under these conditions, late contraction induced by 340-407 mosm/kg was inhibited, whereas contraction induced by 539 mosm/kg was not. Hypotonic solutions evoked a monophasic contraction. Verapamil or Ca²⁺-free conditions inhibited contraction induced by tonicity of 249-266 mosm/kg but not by tonicity of 213 mosm/kg. Hyper- or hypotonicity-induced contractions were not affected by the presence or absence of endothelium. These results suggest that a small increase or decrease in tonicity within the pathophysiological range of osmotic pressure (260–340 mosm/kg) evokes contraction in human umbilical arteries by stimulating calcium influx through voltage-sensitive Ca²⁺ channels.

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Hyperosmolarity: effects on nerves and smooth muscle of cutaneous veins

Cited by 34 publications

References 0 publications

Influence of diabetes on the reactivity of mesenteric microvessels to histamine, bradykinin and acetylcholine

Influence of diabetes on the reactivity of mesenteric microvessels to histamine, bradykinin and acetylcholine

Vascular reactivity in diabetes mellitus: role of the endothelial cell

Contractile Responses in Human Umbilical Arteries to Hyper- and Hypotonic Solutions

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