Reflex effects evoked from the parietal pericardium in the dog: comparison with responses from the visceral pericardium.

Experiments were performed on anaesthetized, open-chest dogs to determine the reflex effects on systemic blood pressure and heart rate produced by stimulation of the parietal pericardium with bradykinin and nicotine, and to compare these effects with those evoked by application of these substances to the visceral pericardium (epicardium) of the left ventricle. Bradykinin (0.01-6.

Prostanoids and cardiac reflexes of sympathetic and vagal origin.

Prostaglandins in concentrations too low to stimulate afferent nerve endings in the heart may sensitize them to chemical or mechanical stimuli that activate cardiac reflexes during myocardial ischemia. Bradykinin, which is released from the heart during ischemia, elicits sympathetically mediated reflex pressor effects and tachycardia when applied in low doses (0.1 to 1 microgram) to the epicardium of the left ventricle in open-chest, anesthetized dogs.

Effects of prostacyclin on cardiovascular reflexes from the ventricular epicardium of the dog: comparison with the effects of prostaglandin E2.

Application of bradykinin to the exposed ventricular surface of the dog's heart produced reflex pressor effects and tachycardia, whereas application of nicotine evoked reflex hypotension and bradycardia. Prostacyclin (PGI2) or prostaglandin E2 (PGE2), when applied epicardially, had no effects by themselves but potentiated the reflex pressor changes to bradykinin; the depressor responses to nicotine were not changed. The potentiating effect of PGI2 was prompt but short-lived, whereas that of PGE2 was slow in onset but prolonged.

Participation of the sympathetic and the renin--angiotensin systems in blood pressure control during hypercapnia in the anaesthetized dog.

The effects of hypercapnia on plasma renin concentration and blood pressure were studied in anaesthetized dogs, untreated and after pretreatment with guanethidine, propranolol or prazosin. An increase in plasma renin concentration which accompanied hypercapnia in untreated dogs was completely suppressed by pretreatment with guanethidine or propranolol. Prazosin significantly reduced but did not abolish renin release during hypercapnia.