Medda B K, Koley J, Koley B
Dysphagia Research Laboratory, Department of Medicine, Medical College of Wisconsin, Milwaukee 53226, USA.
Jpn J Physiol. 1996 Feb;46(1):3-92. doi: 10.2170/jjphysiol.46.83.
Distension of the urinary bladder can cause reflex pressor responses, which appear to be mediated by increased sympathetic activity. We correlated the involvement of the adrenal gland (medulla) itself and adrenosympathetic nerve activities with the viscerovascular reflexes and their role in controlling the reflex response following distension of the urinary bladder. The experiments were performed in 37 chloralose anesthetized cats. It was observed that reflex rise of blood pressure was not affected by intravenous administration of propranolol, indicating that the beta-adrenoceptors (inhibitory effect) were not involved in such reflex. Phentolamine, hexamethonium and guanethidine sulfate completely prevented the reflex action, and comparison of the magnitudes of responses and this inhibitory effect suggests the participation of alpha-adrenoceptors (excitatory effect) as a result of the vasoconstriction that develops during bladder distension. In the present study, we determined that adrenalectomy significantly (p < 0.0001) altered the magnitudes of reflex response during bladder distension. The 10.4% (systolic, p < 0.001) and 10.6% (diastolic, p < 0.01) change in reflex response was mediated directly through adrenomedullary catecholamines, and the 14.8% (systolic, p < 0.001) and 23.8% (diastolic, p < 0.0001) change in vasopressor response was mediated by adrenosympathetic ganglionic activity. The single unit activity from the central cut end of the adrenal sympathetic nerve was recorded for direct evidence. An increase in electrical activity (1-3 to 7-10 spikes/s; p < 0.001) of the adrenal sympathetic nerve with the rise of blood pressure during bladder distension was observed. We concluded that, like other sympathetic nerves, the adrenal sympathetic nerve contributed to the enhancement of blood pressure during bladder distension. This result also explains the partial inhibition of reflex hypertension during bladder distension after adrenalectomy. These studies also conclude that the adrenal gland and adrenosympathetic nerve act as facilitatory modulators in maintaining catecholamine secretion under conditions of stress (urinary bladder distension).
