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PubMed1978

Cholinergic and adrenergic influences upon cat skeletal muscle performance induced by stimulation of the anterior hypothalamus.

The influence exerted by stimulation of the anterior hypothalamus (zone of cholinergic vasodilatation) on the performance of triceps surae during tetanic contraction has been investigated. Hypothalamic stimulation, if combined with indirect muscle stimulation, improves muscle performance, i.e. slows down the rate of decrease of contraction. The effect is abolished by atropine (0.5 mg/kg) and insensitive to propanolol (0.1 mg/kg). The cholinergic influence is only effective if hypothalamic stimulation coincides with the beginning of motor nerve stimulation. In some of our experiments stimulation of the same central structures elicited another influence on muscle performance, associated with the release of adrenaline into the blood. In this case, contrary to the cholinergic influence, the force of contraction increases only when hypothalamic stimulation does not start earlier than 100 s after the initiation of contraction (phase of slow decline of tension). The effect is insensitive to atropine (0.1 mg/kg) and abolished by propanolol (0.1 mg/kg).

Animals↗
PubMed1993

Interaction of myogenic and adrenergic mechanisms in isolated, pressurized uterine radial arteries from late-pregnant and nonpregnant rats.

OBJECTIVE: The purpose of this study was to examine how myogenic and adrenergic mechanisms interact in controlling the lumen diameter of small uterine arteries from nonpregnant and late-pregnant rats. STUDY DESIGN: Radial arteries (150 to 250 microns lumen diameter) from nonpregnant (n = 28) and late-pregnant (n = 18) rats were studied in vitro under conditions of varying transmural pressure and agonist concentrations. RESULTS: (1) Arteries from late-pregnant rats were significantly (p < 0.05) larger in diameter and, unlike nonpregnant vessels, developed a stable intrinsic tone at transmural pressures > 25 mm Hg. (2) Vessels from late-pregnant rats displayed a threefold increase in sensitivity to the constrictor effects of phenylephrine: 50% of maximal constriction, nonpregnant = 691 +/- 148 nmol/L and late-pregnant = 229 +/- 32 nmol/L (p < 0.01). (3) There was no difference in sensitivity to potassium depolarization. (4) Arteries from late-pregnant rats actively constricted to changes in transmural pressure, whereas those from nonpregnant did not unless preactivated beforehand with phenylephrine or K+. (5) After preconstriction the autoregulatory effectiveness of late-pregnant arteries in physiologic saline solution versus phenylephrine or K+, or of nonpregnant in K+ and phenylephrine, appeared to be equal in terms of absolute micrometers but not relative percent change in lumen diameter. CONCLUSION: Pregnancy is associated with significant changes in the active contractile properties of uterine resistance artery function, specifically heightened alpha-adrenergic sensitivity, intrinsic (pressure-dependent) tone, and myogenic reactivity.

Animals↗
PubMed1986

Cardiorespiratory effects produced by microinjecting L-glutamic acid into medullary nuclei associated with the ventral surface of the feline medulla.

The purpose of our study was to use microinjections of L-glutamic acid to better localize the cell bodies in the intermediate area of the ventral medullary surface that exert control over cardiorespiratory activity. L-glutamic acid (200 nl of a 1-M solution) was microinjected into the nucleus paragigantocellularis lateralis, lateral reticular nucleus and into an area which is part of the 'glycine-sensitive area', which lies in the center of the intermediate area. Normally, when L-glutamic acid is applied to the surface of the intermediate area, increases in arterial pressure and tidal volume are observed. Increases in tidal volume were never observed upon microinjection into the 3 sites associated with the intermediate area, suggesting that the tidal volume change elicited from surface application occurs because of L-glutamic acid interacting with cell bodies either on the surface or extremely close to the surface. Pressor responses were elicited with microinjection of L-glutamic acid into the lateral reticular nucleus and the 'glycine-sensitive area', but not the nucleus paragigantocellularis lateralis; indeed, microinjection of L-glutamic acid into the nucleus paragigantocellularis lateralis caused hypotension. Hence, cell bodies responsible for raising arterial pressure may reside in either the lateral reticular nucleus or the 'glycine-sensitive area'.

Animals↗