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Biomedical subjects

G Kaley

Publications and source records attributed to G Kaley.

At least 109 records · Page 6Linked to original sources
PubMed1977

Role of prostaglandins in the mediation of systemic tachyphylaxis to angiotensin II.

Angiotensin-induced prostaglandin release has been implicated in the deveolpment of tachyphylaxis to angiotensin in vitro. Based on these findings and evidence that prostaglandins modulate the angiotensin reposne locally, experiments were done to investigate the role of prostaglandins in the systemic tachyphylaxis to angiotensin. Rats were given intravenous infusions of 1-asparaginyl-5-valyl and 1-aspartyl-5-isoleucyl andiotensin II at two different doses. Using systemic blood pressure as a parameter, varying degrees of tachyphylaxis were produced and the aspartyl analog was found to be more tachyphylactic. When rats were given indomethacin, a prostaglading synthesis inhibitors, the response to intravenous infusion of aspartyl angiotensin was not significantly altered.

Angiotensin II↗
PubMed1977

Arteriolar reactive hyperemia: modification by inhibitors of prostaglandin synthesis.

Several studies implicate endogenously synthesized prostaglandins in the mediation of reactive hyperemic responses in the coronary, renal, and skeletal muscle circulations. We sought additional evidence to involve locally released prostaglandins in the mediation of reactive hyperemia in skeletal muscle at the level of the microcirculation. The cremaster muscle of pentobarbital-anesthetized Wistar-strain rats was prepared for direct in vivo observation and measurement of postocclusive responses of single arterioles. Responses of individual arterioles were reproducible over a 3-h test period. The postocclusion increase in diameter and the duration of response were dependent upon the duration of the occlusion. Repetitive occlusions did not influence arteriolar responsiveness to vasoactive substances. Indomethacin and 5-8-11-14-eicosatetraynoic acid, inhibitors of prostaglandin synthesis, did not affect resting arteriolar diameters; however, both drugs decreased the maximum increase in diameter and duration of the vasodilator response following release of the arteriolar occlusion. These findings suggest that in this microcirculatory bed, prostaglandins contribute little to resting vascular tone; in contrast, temporary arteriolar occlusion elicits the local release of dilator prostaglandins which contribute to the reactive hyperemic response.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1977

Prostaglandins and the control of blood flow in the canine myocardium.

A comprehensive study was undertaken to evaluate the effects of inhibition of prostaglandin (PG) synthesis on a variety of reactions in the coronary vascular bed of anesthetized, open-chest dogs. In 23 dogs an electromagnetic flow probe (EMFP) and hydraulic occluder were placed around either the left anterior descending or circumflex branches of the coronary artery and a needle was inserted distral to the EMFP. Injections into the coronary artery of arachidonic acid (AA), bradykinin, adenosine, angiotensin, and PGE2 were given before and after inhibition of PG synthesis by indomethacin (IND) or meclofenamate (MF). The effects of the inhibitors on reactive hyperemia resulting from 5-, 10-, 15-, and 20-second occlusions and the dilation resulting from 90-second exposure to 8% O2 were also examined. In each experiment, inhibition of PG synthesis was ascertained by the elimination of vasodilation to AA. After administration of IND or MF, while baseline coronary blood flow was slightly reduced, the total increment of blood flow to vasodilator agents was not significantly altered. Whereas the peak dilation and volume of reactive hyperemia were decreased, the percent flow debt repaid was unchanged and total increment of coronary flow due to hypoxia-induced vasodilation was not significantly modified. Vasoconstrictor responses to angiotensin were also unchanged. These results indicate that while inhibitors of PG synthesis increase coronary resistance, they do not adversely affect vascular responsiveness. We conclude that prostaglandins play little, if any, role in modulating coronary blood flow.

Adenosine↗
PubMed1976

Natriuresis induced by intracarotid infusion of hypertonic NaCl.

The intracarotid infusion of hypertonic sodium chloride in anesthetized dogs pretreated with vasopressin and mineralocorticoid resulted in an increase in sodium excretion as well as an increase in the percent of the filtered load of sodium excreted. This increase was not due to changes in renal hemodynamics or arterial blood pressure. The change in fractional sodium excretion was approximately 1%. Intracarotid infusion of isotonic sodium chloride did not result in a natriuretic response. The intracarotid infusion of hyperosmotic glucose did not evoke an increase in sodium excretion. Femoral vein infusions of hypertonic sodium chloride failed to evoke any natriuretic response. These data indicate that a sodium-sensing mechanism may exist in the brain that can alter the renal handling of sodium. The efferent mechanism of the response is discussed.

Animals↗
PubMed1976

Prostaglandins and local circulatory control.

The present paper reviews several lines of investigation have provided highly suggestive evidence for an important regulatory role for prostaglandins in the microcirculation. Aside from their profound vasodepressor effects in a number of animal species, including man, and their vasodilator activity in many local circulatory beds, endogenously administered prostaglandins of the E and A type also appear to reduce vascular responsiveness to a variety of vasoconstrictor agents. Furthermore, inhibition of endogenous synthesis and release of prostaglandins leads to a potentiation of vasoconstrictor responses. Thus it appears that the release of prostaglandins, an event that accompanies or is a consequence of vasoconstriction, can moderate the constrictor response and in this manner can contribute to the control of vascular reactivity. Administration of inhibitors of prostaglandin synthesis to tissues that under basal experimental conditions release prostaglandins, causes not only a decrease in prostaglandin output but also an increase in resting perfusion pressure. These results support the concept that prostaglandins that are released are essential in the control of vascular tone and resistance. Other evidence also suggests that prostaglandins participate in a variety of vascular responses, including the mediation of bradykinin vasodilation, functional hyperemia, and reactive hyperemia.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1975

Inhibition of bradykinin vasodilation and potentiation of norepinephrine and angiotensin vasoconstriction by inhibitors of prostaglandin synthesis in skeletal muscle of the rat.

Recent reports have indicated that vascular responsiveness can be altered by exogenously administered or endogenously released prostaglandins. Furthermore, in certain tissues inhibitors of prostaglandin synthesis have been shown to limit the increase in blood flow in response to bradykinin and to enhance the reduction in blood flow in response to angiotensin and norepinephrine. These findings suggest an important local circulatory role for prostaglandins. We attempted to implicate further prostaglandins in local blood flow regulation by examining the effects of indomethacin (IND) and 5,8,11,14-eicosatetraynoic acid (ETA), inhibitors of prostaglandin synthesis, on microvascular arteriolar responses to bradykinin, prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), histamine, norepinephrine, and angiotensin. Male Wistar rats were anesthetized with sodium pentobarbital, and their cremaster muscle was exteriorized and prepared for in vivo microscopic observation of microvessels. Changes in arteriolar luminal diameters in response to topical administration of vasoactive agents were quantified with an image-shearing measuring eyepiece in conjunction with a television microscope and recorder. Local administration of IND or ETA significantly reduced the arteriolar dilation elicited by bradykinin, whereas the responses to PGE1 and PGE2 remained unaltered. Responses to histamine, although somewhat reduced, were not significantly different from control. Vasoconstrictor responses of arterioles elicited by norepinephrine and angiotensin were potentiated by IND or ETA administration. These results indicate that prostaglandins synthetized in skeletal muscle microcirculation in situ (1) mediate, in part, vasodilator responses to bradykinin and (2) modulate vasoconstrictor responses to angiotensin and norepinephrine. Thus, these findings support the hypothesis that prostaglandins are local regulators of microvascular responsiveness.

5,8,11,14-Eicosatetraynoic Acid↗