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Renal hypertension is better understood now as a result of the development of new laboratory techniques which permit the identification of the surgically curable forms of renovascular and renal parenchymal hypertension. The rationale for and efficacy of these new advances are discussed and a practical approach to the diagnosis of renal hypertension is offered.
Renal tissue from neonatal hamsters was grafted into the cheek pouch of adult hamsters. Renal hypertension was induced in 28 hamsters, and sham operation was performed in 27. When blood pressure became elevated in hypertensive hamsters (10 to 12 days), the renal microcirculation of both groups was evaluated by direct microscopy. Wall and luminal diameter and vascular responses to norepinephrine (NE) and angiotensin II (AII) were determined on glomerular afferent and efferent arterioles and on the corresponding cheek pouch arterioles. In the hypertensive hamsters, the luminal diameter of the afferent arteriole increased, as did the wall/lumen ratio of the efferent arteriole. Although all vessels responded to direct application of NE and AII in both groups, the response of the afferent to AII and the response of the efferent to both NE and AII was greater in the hypertensive hamsters as compared to the sham-operated hamsters. These results indicate that during the development of renal hypertension structural alterations of glomerular vessels and the selective vascular responses to vasoactive agents would lead to an increased glomerular capillary pressure.
Renal hypertension of the two-kidney type is divided into three stages. In the first, hypertension results from the vasoconstrictor effect of angiotensin II. This persists to some extent in the second phase but there is in addition a slow-developing pressor effect, also resulting from angiotensin II and probably attributable to sodium. In the first two phases removal of the abnormal kidney corrects the hypertension. This fails in the third phase because changes in the opposite kidney maintain hypertension. Renin and angiotensin are probably not involved at this stage.
Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.
In conscious and anesthetized normotensive rats, intravenous administration of diltiazem (0.1--3 mg/kg) produced a dose-related decrease in blood pressure. Administration of diltiazem (1--50 mg/kg) into the duodenum of anesthetized rats also reduced the blood pressure in a dose related manner. In parallel with the change in blood pressure, the heart rate increased in conscious rats and decreased in anesthetized animals. Such an increase in the heart rate was suppressed by pretreatment with propranolol. Similarly, in conscious spontaneously hypertensive rats (SHR), diltiazem dose-dependently decreased the blood pressure and increased the heart rate after intravenous administration (0.03--1 mg/kg). Oral administration of diltiazem (100 mg/kg) also reduced the blood pressure of SHR. In addition, the progressive increase in blood pressure in young SHR was significantly suppressed by chronic oral administration of diltiazem (30 mg/kg). The blood pressure in conscious renal hypertensive rats was also decreased with diltiazem (50 mg/kg p.o.). On the other hand, it was demonstrated that the pressor responses to norepinephrine and angiotensin II in the anesthetized normotensive rats were non-competitively inhibited by intravenous administration of diltiazem at a dose which had no effect on the blood pressure.
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Reconstruction of a stenotic renal artery was done on 5 hypertensive renal transplant recipients, all of whom had deterioration of renal function when the stenosis was detected. After reconstruction renal function improved in 4 of the patients. The blood pressure was easier to control in all 5 patients, with 3 becoming normotensive. A high preoperative plasma renin activity returned to normal postoperatively in 4 patients. No recurrences were observed after a followup of more than a year.
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Renal hypertension was produced in 14 Sprague-Dawley rats by ligating both poles of one kidney followed in one week by unilateral nephrectomy. Biweekly subcutaneous injections of SQ 20858 reduced the blood pressure in the chronic renal hypertensive animals. Upon discontinuing the injections the blood pressure rose to pretreatment levels. No angiotensin II activity was seen in seven of the renal group treated with SQ indicating a complete block in serum converting enzyme activity. Likewise, serum with only angiotensin I activity when added to normal serum containing converting enzyme, continued to show angiotensin I activity. It is concluded that SQ 20858 is effective in lowering blood pressure in chronic renal hypertensive rats presumably by partially inhibiting converting enzyme.
1. After 4.5 months of renal hypertension in rats renal artery 'declipping' was performed. Eight weeks afterwards paired hindquarter perfusions were performed on the declipped rats and normotensive control rats, exploring the relationships between mean arterial pressure and flow, from maximal vasodilatation to maximal vasoconstriction, induced by graded noradrenaline infusions. Left ventricular weights were measured. 2. Declipping caused a fall in mean arterial pressure from 180 to 135 mmHg, though still after 8 weeks the mean pressure was 19% higher than in normotensive control rats. 3. All parameters reflecting design and reactivity of the resistance vessels and left ventricular weight decreased significantly, but not as much as mean arterial pressure, and were still significantly increased compared with those of control rats. 4. This neither mean arterial pressure nor cardiovascular design was normalized 8 weeks after 'reversal' of long-standing renal hypertension, in contrast to short-standing renal hypertension where both are completely normalized 3 weeks after declipping.
To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 +/- 8 mm Hg) showed significant cardiac hypertrophy (44 +/- 1% increased ratio of heart weight to body weight, P less than 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 +/- 0.8 vs. 4.7 +/- 0.4 mm Hg). We evaluated cardiac function by recording left ventricular end-diastolic pressure, stroke volume (SV), and cardiac output (CO) (by electromagnetic flowmeter) during rapid alteration in venous return. Analysis of variations of stroke volume vs. left ventricular end-diastolic pressure showed that renal hypertension is accompanied by a significant decrease in ventricular performance [SV = 0.0190 + 0.0509 LVEDP - 0.0025 (LVEDP)2 + 0.0001 (LVEDP)3] compared to the normotensive group [SV = 0.0430 + 0.0644 LVEDP - 0.0040 (LVEDP)2 + 0.001 (LVEDP)3]. The alterations in stroke volume and cardiac output were associated with a lack of significant changes in the work performed at matched end-diastolic pressures. The data indicate that chronic renal hypertension is accompanied by a depression of cardiac reserve which is not revealed by measurements of cardiac output and left ventricular end-diastolic pressure at rest. This impairment in cardiac function might be related to either diminished cardiac contractility or reduced left ventricular compliance; the latter possibility is in accord with our finding of a 2-fold increase in the hydroxyproline content (P less than 0.001) and a significant decrease in the DNA concentration of ventricular tissue.
1. Mean arterial pressure, heart rate, cardiac output (dye-dilution technique), stroke volume, total peripheral resistance (TPR), utero-placental blood supply (microsphere technique) and foetal weights were determined 2 days before expected birth in normotensive control (NC) rats, spontaneously hypertensive (SH) rats, rats with short-standing renal hypertension induced early in pregnancy and rats with established renal hypertension induced 4 weeks before pregnancy. Non-pregnant rats in comparable states served as controls. 2. In normal pregnancy cardiac output increased by 33% and blood pressure and TPR decreased by 17 and 38% respectively. The same principal changes were noted in SH rats and those with short-standing renal hypertension, but no changes were found in rats with established renal hypertension during pregnancy. 3. Myometrial and placental blood supply was lower in all hypertensive groups compared with NC rats, the reduction being 46 and 36% in SH rats and in rats with established renal hypertension as much as 74 and 68% respectively. 4. In SH rats foetal weights were reduced compared with NC rats, but despite the 68% reduction of placental blood flow in rats with established renal hypertension foetal weights were here unchanged.
There are different types of renal hypertension: hypertension due to parenchymal renal disease, renovascular hypertension, hypertension due to urological disease, hypertension of endstage renal disease. Treatment has to consider-above all-the possibility of specific, medical or surgical procedures that may cause the underlying condition. If the underlying disease is not amenable to specific therapy, symptomatic medical treatment to lower blood pressure is indicated: besides control of sodium-intake and body weight antihypertensive drugs are generally indicated. We use them, alone or in combination, in the following line of order: diuretics, beta-adrenergic blockers, dihydralazine, reserpine, clonidine, alpha-methyldopa, guanethidine.
1. Biosynthesis and deposition of collagen, as well as DNA and total proteins, are increased in aortae of rats after 1, 3 and 6 weeks of hypertension. 2. The maximal increase in the rate of synthesis of collagen is observed within one week of hypertension when the stress to the arterial wall is maximal. 3. Reserpine administration prevents hypertension and inhibits the increase of collagen metabolism. 4. At any time of evolution of the hypertension, a linear positive correlation is found between the collagen content in the aorta and the level of blood pressure. 5. These data suggest that synthesis of matrix components by the arterial smooth-muscle cells is controlled by variation in the blood pressure level and is not a direct consequence of circulating humoral factors liberated by the ischaemic kidney.
1. Chronic renovascular hypertension developed in uninephrectomized, sodium-depleted dogs in association with a decrease in cardiac output. 2. With sodium and volume repletion of these animals, cardiac output returned to normal but the high level of arterial pressure was unchanged; consequently, the peripheral arterioles dilated. 3. These observations provide evidence against the theory of whole-body autoregulation.
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The rats with chronic renal hypertension caused by constricting one renal artery, exhibit a decrease in the activity of Na-K-ATPase in the outer medulla of the "untouched" kidney, as compared to this activity in the kidneys of intact normotensive rats and in the "untouched" kidney of the rats where renal artery constriction did not result in hypertension. There were no differences between the control normotensive Wistar rats and the spontaneously hypertensive rats (SHR) in the prehypertensive and early hypertensive stages (at the age of 6-8 weeks) as far as the activities of Na-K-ATPase and oxidoreductases (SDH and LDH) in the renal cortex, the outer and inner medulla are concerned. The spontaneously hypertensive rats with chronic hypertension had at the age of 16-20 and 27-29 weeks lower activity of Na-K-ATPase, SDH, and LDH in the outer renal medulla than the control normotensive Wistar rats. The experimental results indicate that in chronic arterial hypertension there is a decrease in the activity of Na-K-ATPase, in the outer renal medulla, which suggests a reduction in the resorpo sodium and water.
The hypotensive actions of dl-propranolol and a new beta-blocking agent, dl-tert-butylamino-3-(2', 3'-dimethylphenoxy)-2-propanol hydrochloride (D-32) were studied in conscious normotensive and renal hypertensive dogs, using a cross-over design. The effects were compared with that of placebo (lactose 200 mg/head, p.o.) administered in a blind fashion. A marked reduction in systolic blood pressure, from 158 +/- 2.9 to 124 +/- 2.3 (mean +/- S.E.) mm Hg, was observed at 3 hr after administration of 50 mg/kg, p.o. of D-32 in renal hypertensive dogs but not in normotensive ones. In both normotensive and renal hypertensive dogs, 10 and 50 mg/kg, p.o. of D-32 caused a marked increase in heart rate. Intravenous infusion of p-OH D-32, a main metabolite of D-32 in dogs, at a rate of 1 mg/kg per min for 5 min into renal hypertensive dogs caused a significant, long-lasting fall in blood pressure and a sustained increase in heart rate, whereas that of D-32 (1 mg/kg per min for 5 min) failed to do so. Propranolol (10 and/or 50 mg/kg, p.o.) produced no significant changes in blood pressure and heart rate in both preparations. These results indicate that D-32 causes a fall in blood pressure in conscious renal hypertensive dogs mainly by a metabolite of D-32, p-OH D-32.