The effects of stimulating carotid chemoreceptors on renal haemodynamics and function in dogs.

Abstract

SUMMARY1. Dogs were anaesthetized with chloralose and artificially ventilated. The carotid chemoreceptors were stimulated by changing the perfusion ofvascularly isolated carotid sinus regions from arterial to venous blood. The mean carotid sinus pressure and the mean arterial blood pressure were held constant at 124 + 3 and 122 + 3 mmHg, respectively. Both vagosympathetic trunks were sectioned in the neck and propranolol (17 ,tg kg-' min-' i.v.) and gallamine triethiodide (0-2-2 0 mg kg-' 30 min-' i.v.) were infused. Renal blood flow was measured by an electromagnetic flow probe, glomerular filtration rate by creatinine clearance, sodium excretion by flame photometry and solute excretion by osmometry.2. In sixteen tests in thirteen dogs perfusion of the carotid sinus regions with venous blood resulted in significant decreases in renal blood flow from 271+24 to 198 + 21 ml min-1 100 g-1 renal mass; glomerular filtration rate from 41-0 + 4-8 to 22-1 + 3-1 ml min-' 100 g-; filtration fraction from 0-25 + 0-02 to 0 19 + 0-02; urine flow from 0-48 + 1-0 to 0-21 + 0-03 ml min-1 100 g-'; sodium excretion from 18-1 + 4-1 to 12-9 + 4-2 #smol min-' 100 g-; and osmolar excretion 327 + 42 to 171 + 26 posmol min-1 100 g-'. The right atrial pressure did not change significantly from 4-6 + 1P2 cmH20.3. In seven dogs, tying renal sympathetic nerves abolished all the responses except that of sodium excretion which was now reversed; sodium excretion increased from 68+19 to 116 + 38 /tmol min-1 00 g-1 without significant change in right atrial pressure from 7-4 + 1-9 cmH2O. Crushing the carotid bodies, however, abolished all the responses.4. The results show that carotid chemoreceptor stimulation can cause significant reflex effects on renal haemodynamics and function which are mediated via renal sympathetic nerves. They also show that the chemoreceptor stimulation can cause natriuresis in the absence of haemodynamic changes, in the denervated kidney, presumably via a humoral factor.

The renal response to electrical stimulation of renal efferent sympathetic nerves in the anaesthetized greyhound.

“…Linden et al (1981) also observed that carotid chemoreceptor stimulation with venous blood caused changes in the renal nerve activity of about 1 Hz. However, in our study of the carotid chemoreflex (Karim et al 1987), the changes in renal nerve activity must have been greater, because both renal haemodynamics and function changed significantly, particularly when a natriuretic factor seemed to be working against the neural action.…”

“…However, in our reflex studies with intact kidneys, initial carotid sinus pressure was set to high, medium or low levels within the baroreceptor sensitivity range (Karim et al 1984(Karim et al , 1987(Karim et al , 1989bKarim & AlObaidi, 1990;Karim & Majid, 1990) and thus the reflex alteration of the renal nerve activity commenced from some basal on-going activity (Kendrick, Oberg & Wennergren, 1972;Linden, Mary & Weatherill, 1981). Although few studies have measure renal nerve activity in response to changes in carotid baroreceptor and chemoreceptor activities (Kezdi & Geller, 1968;Karim, Kidd, Malpus & Penna, 1972;Linden et al 1981), one has attempted to correlate sinus pressure (baroreceptor activity) with renal nerve activity and haemodynamics in the anaesthetized cat (Kendrick et al 1972).…”

“…We have previously reported that the renal haemodynamics and function of dogs can be influenced by stimulation of baro-and chemoreceptors in the carotid sinus regions (Karim, Poucher & Summerill, 1984, 1987, 1989b and atrial receptors (Karim, Majid & Summerill, 1989b). These responses were abolished following ligation of the renal nerves.…”

Primary effects of carotid chemoreceptor stimulation on gracilis muscle and renal blood flow and renal function in dogs.

“…These responses were claimed to be solely due to an inhibition of tubular sodium reabsorption, and were independent of the integrity of vagus nerves and renal haemodynamic and blood pressure changes. However, in anaesthetized vagotomized and artificially ventilated dogs, chemoreceptor stimulation produced antinatriuresis and antidiuresis when the systemic blood pressure was adequately controlled (Karim et al 1987). So far as we know there has been no systematic and comparative study in which the primary effects of physiological stimulation of carotid chemoreceptors on skeletal muscle and renal blood flow and function have been investigated, and the direction and magnitude of secondary changes in these variables from the increase in blood pressure have been determined.…”

“…In fourteen dogs, with sectioned vagosympathetic trunks and controlled AoP, carotid chemoreceptor stimulation caused significant decreases in RBF of 19-1+1-6% (n = 14, P < 0001), in GFR of 17-7+2-2% (P < 0-001), in V of 23-4+2-5% (P < 0-001), in UNaV of 22-0+2-4% (P < 0-001) and in Uosm V of INTRODUCTION It is known that stimulation of the carotid chemoreceptors in anaesthetized and artificially ventilated dogs increases systemic arterial blood pressure and total peripheral vascular resistance (Daly & Scott, 1962, 1963, and renal vascular resistance (Little & Oberg, 1975;Mancia, 1975;Kappagoda, Karim & Mackay, 1983;Karim, Poucher & Summerill, 1987). However, the effect of carotid chemoreceptor stimulation on the skeletal muscle blood flow is still controversial: Mancia (1975) observed that when the hindlimbs were perfused at a constant pressure, carotid chemoreceptor stimulation with hypoxic and hypercapnic blood produced about 60% decrease in hindlirnb blood flow in chloralose-anaesthetized, artificially ventilated and vagotomized dogs.…”