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Biomedical subjects

J T Shepherd

Publications and source records attributed to J T Shepherd.

At least 127 records · Page 7Linked to original sources
PubMed1975

Modification of vagal depressor reflex by CO2 in spontaneously breathing rabbits.

The control of hindlimb and renal vascular beds by vagal afferents was studied, in anesthetized spontaneously breathing rabbits in which the carotid sinus and aortic depressor nerves were cut, by measuring the increase in vascular resistance (constant-flow perfusion with autologous blood) during bilateral vagal cold block (VCB). The effect of hypercapnia was studied with both increased ventilation (caused by inspiration of mixtures of CO2 in O2) and decreased ventilation (caused by infusion of gallamine during O2 breathing). The increase in hindlimb resistance with VCB was correlated with respiratory minute volume but not with PCO2; the reverse was true for the increase in renal resistance. Without VCB the renal vessel constriction caused by the hypercapnia was markedly attenuated, provided that there were minimal respiratory movements; the resistance increased dramatically when these movements were abolished or with VCB. Thus, the powerful central effect of CO2 on the renal vessels can be counteracted by vagal afferents activated by lung movement; even minimal respiratory activity can cause this effect.

Animals↗
PubMed1975

Vasomotor inhibition in rabbits by vagal nonmedullated fibers from cardiopulmonary area.

In anesthetized rabbits with sinus and aortic nerve cut, when the cervical vagal nerves were cooled to 12, 8, 6, and 0degreeC, there were progressive increases in aortic blood pressure of 7 +/- 1, 15 +/- 2, 25 +/- 1, and 41 +/- 2 mmHg (SE), respectively. For comparison, during cooling of the aortic and vagal nerves, at 12degreesC there was a decrease in firing in the afferent fibers from aortic baroreceptors (48 +/- 4%) and pulmonary stretch receptors (57 +/- 5%), and at 6degreesC all activity was abolished. Thus, at 6degreesC the activity in medullated fibers from the aortic baroreceptors and pulmonary stretch receptors is blocked, but the increase in aortic blood pressure with vagal cooling is only 60% of that with cooling to 0degreeC. This demonstrates that cardiopulmonary receptors with nonmedullated vagal afferents (C fibers) contribute to the tonic inhibition of the vasomotor center. Because of overlap in sensitivity of different vagal fibers to cooling, the total contribution of these C fibers cannot be evaluated.

Animals↗
PubMed1975

Continuous inhibition of renin release in dogs by vagally innervated receptors in the cardiopulmonary region.

Inhibition of the release of renin by vagal afferents from the heart and lungs was studied in 14 dogs with their aortic nerves cut and their carotid sinuses vascularly isolated. The release of renin from one kidney was calculated from the venous-arterial difference in plasma renin activity (radioimmunoassay) and the renal blood flow (electromagnetic flowmeter). Renin release was determined before and during temporary interruption of afferent vagal nerve traffic (bilateral cooling of the cervical vagi). With carotid sinus pressure maintained at 40 mm Hg, vagal cooling increased mean aortic blood pressure (24%), decreased renal blood flow (19%), and increased renin release (241%). With sinus pressure maintained at the mean aortic blood pressure existing during the control period, vagal cooling caused a lesser increase in mean aortic blood pressure (12%), little decrease in renal blood flow (7%), and a marked increase in renin release (522%). The changes in renal blood flow and renin release with vagal cooling were prevented by renal denervation. Thus, vagal afferents from the cardiopulmonary region exert a tonic restraint on the release of renin; this restraint occurs in circumstances in which these afferents cause little change in total renal blood flow.

Angiotensin II↗
PubMed1975

Role of cardiac, pulmonary, and carotid mechanoreceptors in the control of hind-limb and renal circulation in dogs.

Reflex control of hind-limb and renal resistance vessels by cardiac and pulmonary receptors was studied by interrupting afferent vagal nerve traffic when only the heart or only the lungs were in situ in anesthetized dogs with sinoaortic denervation. During normocapnia, interruption of cardiac and of pulmonary vagal traffic decreased hind-limb blood flow (constant-pressure perfusion) by 23% and 21%, respectively. Corresponding decreases in renal blood flow were 23% and 33%. Hypercapnia augmented the decreases in renal blood flow due to the vagal block. Thus, the inhibitions exerted by the heart and lung receptores on these two beds were similar during normocapnia but were greater on the renal vessels during hypercapnia. In closed-chest dogs with their aortic nerves sectioned and their carotid sinus pressure controlled, combined withdrawal of carotid and cardiopulmonary inhibition decreased hind-limb and renal blood flow by about 80% and 40%, respectively, during both normovolemia and hypervolemia. Interruption of cardiopulmonary inhibition was responsible for 17% and 31% of the decrease in hind-limb blood flow at normal and increased blood volumes, respectively; values for the decreases in renal blood flow were 50% and 65%. Thus, cardiopulmonary receptors oppose the vasoconstriction due to carotid hypotension more effectively in the kidney than they do in the hind limb.

Animals↗
PubMed1975

[Vascular reflex responses during skeletal muscle contraction in dogs].

Electrical stimulation of the muscles of the thigh in the anaesthetized dog induces reflex changes of the aortic pressure and of the renal vascular tone. The afferent pathways is located in the somatic nerves of the stimulated limb, the efferent pathways is in the ortosympathetic nerves. Muscle contraction is necessary to activate the receptors, responsible for the reflex increase of the arterial pressure; this contraction is not necessary to activate the receptors responsible for the blood pressure decrease. It is probably that the former receptors play a role in the increase of the sympathetic tone during muscle exercise.

Afferent Pathways↗