Search

Hindquarter (terminal aortic) blood flow (HQF) and arterial pressure (AP) were observed in rats with an electromagnetic flow probe implanted around the terminal aorta and an arterial indwelling cannula. Hindquarter peripheral resistance (HQR) was calculated by dividing mean AP by HQF. Under pentobarbital anesthesia, HQR was decreased significantly (p less than 0.001) by ganglionic blockade with hexamethonium bromide (C6). Since C6 does not change HQR significantly without anesthesia, we interpret that pentobarbital anesthesia generated a sympathetic vasoconstrictor tone in hindquarter resistance vessels. This was further substantiated by the observation that the increase in HQR on infusion of vasopressin was obscure under pentobarbital anesthesia: Presumably, the increase was offset by reflex inhibition of the hindquarter tone induced by anesthesia. The generation of hindquarter vasoconstrictor tone by pentobarbital was for the most part ascribable to the baroreceptor reflex to compensate for the depressor effect of this anesthetic, because it was greatly diminished after severance of the buffer nerves.

Mean arterial pressure and three regional blood flows--renal, superior mesenteric, and hindquarter flows--were monitored in conscious normotensive control rats (NCR), in two-kidney, one-clip (two-kidney), and in one-kidney, one-clip (one-kidney) hypertensive rats. After administering captopril, an angiotensin-converting enzyme inhibitor, mean arterial pressure decreased in all three groups. However, lowering of arterial pressure was not statistically significant in any of the groups. Renal flow increased significantly in the intact artery of two-kidney hypertensive rats, whereas it did not significantly increase in the clipped artery of one-kidney hypertensive rats and in the intact artery of NCR. Superior mesenteric flow increased significantly only in one-kidney hypertensive rats. Hindquarter flow did not significantly change in the three groups. Regional resistance reduced significantly in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it did not reduce significantly in these two vascular areas in one-kidney hypertensive rats and in NCR. The present findings show that the renin-angiotensin-mediated vasoconstriction plays a role in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it hardly plays a role in these three vascular beds in one-kidney hypertensive rats.

Changes in blood flow in different arteries occurring in the transposition response of the rat, induced by transposing the animal from a "home" cage to a new one, were studied using chronically implanted electromagnetic flow probes. In the response, hindquarter flow was increased by more than 50%, superior mesenteric and renal flows were decreased by about 30 and 15%, respectively, and common carotid flow remained almost unchanged. The increase in hindquarter flow in the response was much less after beta-adrenoceptor blockade with propranolol. In adrenalectomized rats the flow changes in the hindquarter, mesenteric, and renal areas were less marked in either direction. These findings indicate that the blood flow redistribution in the transposition response is characterized by a shift of flow from the viscera to the skeletal muscles, in which the alpha- and beta-effects of catecholamines released from the adrenal medulla in the response play a dominant role.

Aortic flow and arterial pressure were observed in conscious rats by means of an electromagnetic flowmeter probe implanted around the ascending aorta and an arterial cannula inserted into the abdominal aorta through a femoral artery. When the rat was transposed to a new box from its usual one, heart rate, cardiac output and peak flow acceleration were increased but arterial pressure remained unchanged. Total peripheral resistance was decreased. This response complex of the cardiovascular system to change of habitat was designated as "transposition response." After beta adrenoceptor blockade with propranolol, transposition no longer increased heart rate, cardiac output or peak flow acceleration but markedly increased arterial pressure and total peripheral resistance. The response was essentially unchanged by atropinization or adrenalectomy. Besides cardiac excitation and adrenergic vasoconstriction, the response includes a beta adrenergic vasodilatation, which is at least in part mediated by transmitters released at the sympathetic nerve endings and presumably equivalent to the cholinergic vasodilatation in the cat and dog.

Blood flow in the terminal aorta or superior mesenteric artery was recorded in conscious one-clip, two-kidney renovascular hypertensive rats and normal control rats with a chronically implanted electromagnetic flow probe. An indwelling catheter for direct measurement of arterial pressure was inserted into the terminal aorta in rats with a flow probe around the superior mesenteric artery. In the hindquarter area supplied by the terminal aorta, the elevation of vascular resistance in hypertensive rats in relation to normal rats was close to the average over the whole body. However, it was about 40% more intense than the average in the superior mesenteric area. Quantitatively, the hindquarter and superior mesenteric beds in hypertensive rats contributed about a quarter and a third of the decrease in total vascular conductance, respectively. Plots of superior mesenteric flow per body weight against arterial pressure at rest for 51 measurements in 9 hypertensive rats revealed an inverse relation between these two variables. These findings indicate that elevation of vascular resistance in the superior mesenteric area and probably the splanchnic area in general play an important role in one-clip, two-kidney renovascular hypertension.

Using an electromagnetic flowmeter, regional blood flow was measured at the carotid, celiac, superior mesenteric, renal, and iliac arteries in normal Wistar rats and spontaneously hypertensive rats anesthetized with pentobarbital sodium. The sum of the mean values of the flow rate normalized per 100 g body weight for all the arteries was similar for both groups. About a half of the sum was drained through the superior mesenteric artery in both groups. The normalized flow rate was similar for both rat groups for each artery excepting the renal artery where the flow rate was significantly greater in the hypertensive rats.

Cardiovascular response in an alerted state induced by vibration was studied in conscious rats by giving a to-and-fro movement to their cages for 30 sec. Cardiac output, superior mesenteric flow, and hindquarter flow were observed with chronically implanted electromagnetic flow probes and arterial pressure with an indwelling catheter. Arterial pressure, heart rate, cardiac output and hindquarter flow increased and superior mesenteric flow decreased with vibration. The increase in heart rate was still present after adrenalectomy, but was abolished by beta-adrenoceptor blockade propranolol. The increase in hindquarter flow was greatly diminished by propranolol or after adrenalectomy, but was still present in adrenalectomized rats after alpha-adrenoceptor blockade phentolamine. The decrease in superior mesenteric flow in vibration was abolished by phentolamine. It was diminished by adrenalectomy. These findings indicate that the cardiovascular response to vibration includes excitation of the cardiac sympathetic nerves, adrenomedullary secretion, and excitation of sympathetic vasoconstrictor fibers and exercise hyperemia in skeletal muscles.

Three regional blood flows were measured in one-kidney, one-clip renovascular hypertensive (one-kidney hypertensive) rats with chronically implanted electromagnetic flow probe. One-kidney hypertensive rats showed about 30% greater superior mesenteric flow, about 20% greater hindquarter flow at the terminal aorta, and an almost unchanged renal flow at the clipped renal artery when compared with control rats, but the sum of the mean values of these three regional blood flows in one-kidney hypertensive rats was almost the same as that of control rats. One-kidney hypertensive rats had a higher peripheral resistance in all the investigated vascular areas. The increase in peripheral resistance of the renal area including the clipped and removed arteries was greater than that in peripheral resistance of the superior mesenteric area or hindquarter area. These findings suggest that the remaining renal area which failed to compensate for the flow deprived by uni-nephrectomy plays a role in the etiology of this kind of hypertension.