Haemodynamic and other studies on the renoprival hypertensive rat

Abstract

SUMMARY1. The optimal conditions for the development of hypertension after total nephrectomy were defined in the rat. Under these conditions, haemodynamic changes were then studied before and for 3 days after total nephrectomy in the unanaesthetized animal and compared with mocknephrectomized controls.2. Changes in cardiac output were followed with an electromagnetic flowmeter chronically implanted on the ascending aorta, and mean arterial pressure with an indwelling aortic cannula.3. Haematocrit fell in animals developing hypertension, due to plasma volume expansion. Restriction of administered saline did not reduce the fall in haematocrit without also preventing development of the hypertension.4. Cardiac output and stroke volume increased significantly on the second and third days after nephrectomy. Peripheral resistance remained unchanged and pulse rate tended to fall.5. The increase in cardiac output appeared to be more than could be accounted for by anaemia alone, and it is suggested that plasma volume expansion was partly responsible.6. In another group of rats developing renoprival hypertension a correlation was found between changes in plasma volume and arterial pressure over the three days.7. Renoprival hypertension was accompanied by a slight but significant reduction in oxygen consumption in comparison with the controls. 8. No relationship was found between the changes in blood pressure, and plasma sodium and potassium levels.9. It is concluded that the observed rise in cardiac output associated with renoprival hypertension as induced in this study was not attributable to anaemia nor to a rise in metabolic rate. The implications of this situation are discussed in relation to a theory of the pathogenesis of hypertension and the findings of other workers.

Animal models for the study of arterial hypertension

“…Removal of one kidney and approximately two-thirds of the other is followed by a slow increase in BP. In these animals, intravascular volume increases and the resulting hypertension may have the same pathogenesis as renoprival hypertension (Ledingham and Pelling 1970). Since a bilateral nephrectomy leads to hypertension with vascular lesions, especially if the animal's life is prolonged after the complete removal of the kidneys (Ferrario et al 2009).…”

Renal Control of Changes in the Compliance of the Interstitial Space: A Factor in the Aetiology of Renoprival Hypertension

“…Green (1969) also observed a different distribution of fluid between the vascular compartment and the interstitial space; the plasma/extracellular fluid (PV/ECFV) ratio was significantly higher after bilateral nephrectomy (BN) than after unilateral nephrectomy and ureterocaval anastomosis (UNUCA). Ledingham & Pelling (1970) have shown in rats that hypertension after bilateral nephrectomy (renoprival hypertension) is associated with increased plasma volume and increased cardiac output; peripheral resistance remains normal or falls. Since expansion of the blood volume after unilateral nephrectomy and ureterocaval anastomosis does not cause a rise in blood pressure, either peripheral resistance must decrease or cardiac output must remain normal after this procedure.…”

Effects of aerobic exercise training in animal models of hypertension.

“…In this model, the increased intravascular volume results in hypertension and may have the same renopriva pathogenesis of hypertension. (60) SHR animals subjected to 5/6 nephrectomy for removal of the left kidney and removal of two-thirds of right kidney, underwent APT treadmill for 4 weeks of moderate intensity, observing attenuation of proteinuria and protection to increased glomerular sclerosis. (61) However, the APT associated with enalapril or losartan reduced the BP and induced significant additional protection against an increase in glomerular sclerosis.…”