Urinary bladder distension: its effects on carotid baroreceptor reflex left ventricular inotropic response in the dog.

Abstract

1. The effects of distension of the urinary bladder on heart rate, maximum rate of change of left ventricular pressure (dP/dt max) and hindlimb vascular resistance together with their modulation at different carotid sinus pressures were studied in dogs anaesthetized with a mixture of chloralose and urethane and artificially ventilated. 2. When the carotid sinus mean perfusion pressure was raised in randomly selected steps from 60 to 210 mmHg, it caused a progressive bradyeardia, and a reduction in left ventricular dP/dt max and in arterial blood pressure, together with vasodilatation in the perfused hindlimb. Distension of the bladder at each level of carotid sinus pressure resulted in tachyeardia, a small but significant increase in left ventricular dP/dt max (160 + 30 mmHg s-') and hindlimb vasoconstriction.3. When heart rate and arterial blood pressure were held constant to exclude these secondary effects on left ventricular dP/dt max, raising the carotid sinus pressure caused a progressive reduction in left ventricular dP/dt max and hindlimb vasodilatation. Superimposition of tests of bladder distension at each level of sinus pressure resulted in variable responses, but overall there was a significant increase in left ventricular dP/dt max of 190 + 54 mmHg s-. Hindlimb vasocontriction, however, was a consistent finding. 4. The gain of the relationship between the carotid sinus perfusion pressure and left ventricular dP/dt max was unaffected by distension of the bladder. 5. It is concluded that, when changes secondary to increases in heart rate and blood pressure are prevented, distension of the bladder causes a small but significant reflex increase in left ventricular dP/dt max. The responses, however, are variable and the possible reasons for this are discussed.

GABAergic control of micturition within the periaqueductal grey matter of the male rat

“…This reversal could have been due to sympathetic redistribution of blood flow during bladder stretch leading to an increase in blood pressure, which masked any depressor response caused by a decrease in GABAergic inhibition in the cvlatPAG during micturition. This pressor response during bladder stretch has been demonstrated in man as well as in cats and dogs (Guttmann & Whitteridge, 1947;Cunningham et al 1953;Mukherjee, 1957;Weaver, 1985;Ward et al 1995).…”

“…This pressor response during bladder stretch has been demonstrated in man as well as in cats and dogs (Guttmann & Whitteridge, 1947; Cunningham et al . 1953; Mukherjee, 1957; Weaver, 1985; Ward et al . 1995).…”

Respiratory modulation of carotid and aortic body reflex left ventricular inotropic responses in the cat

“…However, simultaneous changes in other variables, notably heart rate and arterial blood pressure can also affect left ventricular d P /d t max directly (Bowditch, 1871; Anrep, 1912; Starling, 1918; Sarnoff, Mitchell, Gilmore & Remensnyder, 1960; Furnival et al 1970), and, therefore, if not controlled can vitiate the interpretation of any reflex changes resulting from stimulation of the arterial chemoreceptors. Furthermore, changes in blood pressure can reflexly affect left ventricular contractility through an arterial baroreceptor reflex (Hainsworth & Karim, 1972, 1973; Ward et al 1995). By carrying out the present study under conditions in which the heart was electrically paced and the arterial blood pressure was maintained constant, the secondary effects on left ventricle d P /d t max of changes in heart rate, arterial blood pressure and arterial baroreceptor activity were eliminated.…”

“…The reason for this was that stimulations of the carotid and aortic bodies invariably cause increases in vascular resistance as primary reflex vascular responses (Daly & Ungar, 1966; see also Daly, 1997, chapters 9 and 10). Thus, these vascular responses provide a valuable means of monitoring the viability of preparations when the response of the main variable under consideration is weak or ephemeral, as for instance, in the study of the left ventricular inotropic responses occurring on distension of the urinary bladder (Ward et al 1995). In the present experiments, responses of the hindlimb, apart from providing information on the reflex activity of the preparations when the left ventricular inotropic effects of stimulation of the arterial chemoreceptors were abolished by propranolol, also acted as a guide as to the doses of the chemical agent to be used for exciting the two groups of chemoreceptors.…”

“…This increased resistance to ventricular injection per se is known to increase ventricular contractility (Anrep, 1912). Furthermore any rise in arterial blood pressure would, through an arterial baroreceptor reflex, exert the opposite effect on contractility (Hainsworth & Karim, 1972, 1973; Ward, Daly & Wood, 1995). De Geest, Levy & Zieske (1965) also reported that stimulation of the carotid bodies had a negative inotropic effect on the left ventricle but they attributed it to an increase in vagal activity.…”