Reversal of renovascular hypertension: role of the renal medulla

The fall in blood pressure, which occurs when renovascular hypertension is corrected surgically, offers a means of elucidating the factors responsible for blood pressure control. When Goldblatt two-kidney, one-clip hypertension in the rat is reversed by unclipping the renal artery, or by removal of the ischaemic kidney, restoration of normal blood pressure is due to a fall in peripheral resistance. This is associated with sodium retention and cannot be modified by inhibition of the renin-angiotensin system. The fall is, however, partially inhibited by chemical removal of the renal medulla by means of 2-bromo-ethylamine hydrobromide. When normal rats are chemically medullectomized, moderate hypertension is produced, which cannot be attributed to the renin-angiotensin system or sodium retention. It is concluded that a renomedullary vasodepressor system is ablated by chemical medullectomy: further, this system plays a role in the surgical correction of Goldblatt hypertension.     

Radiologic endovascular prosthesis of the renal arteries in patients with renovascular hypertension]

A high percentage of restenoses after roentgenovascular dilatation of the renal arteries laid the basis of a search for new therapeutic methods for these patients. Experiments on implantation of nitinol spiral endoprostheses showed their ability for long-term permeability of renal arteries, not causing their thrombosis and intimal spreading, destruction of formed elements of the blood, change in plasma proteins. Morphological investigations have shown rapid formation (during 14 days) of connective tissue neointima, covered on the side of the blood flow with the true vascular endothelium (ensuring a nonadhesive surface and laminar blood flow), around the coils of an endoprosthesis. This method after its experimental development started to be used in clinical practice. The authors reported the first experience in the clinical use of this method (12 patients with vasorenal hypertension). A 15-month follow-up revealed a stable antihypertensive effect in all patients.     

Ultrastructural changes of the rat renal glomeruli in the early phase of renovascular hypertension

Electron microscopic studies were carried out on rat kidneys during the early phase of "two-kidney" Goldblatt hypertension. Pathologic ultrastructural changes (confluence of foot processes of the podocytes, formation of intercellular juctions between them, etc.) and an enhanced permeability to ferritin were found in the glomeruli of both the ischaemic and the contralateral kidneys. Signs of activation and exhaustion of the lysosomal system appeared in the glomerular epithelial cells of the untouched kidneys. These signs were absent in the kidneys with constricted arteries. The possible significance and pathogenesis of the alteration are discussed in comparison with other pathological conditions showing a similar ultrastructural picture.     

Reconstructive vascular surgery for renovascular hypertension

Forty-six patients who underwent renal artery repair for presumptive renovascular hypertension are presented. Preoperative investigation included a rapid sequence IVP, a high quality angiogram and split function studies, as well as renin assays of renal venous blood in the more recent cases. Atherosclerosis was the causative pathological lesion in 60% of the patients, with fibromuscular dysplasia or miscellaneous causes of stenosis accounting for the remaining 40%.Surgical correction was usually obtained by bypass grafting (57%). Hypertension was cured or significantly improved in 36 patients (78%).Optimal results are dependent upon complete preoperative investigation and surgical repair of all the stenotic areas.     

Renal actions of angiotensin II in renovascular hypertension

In renal artery stenosis severe enough to cause hypertension, angiotensin II maintains glomerular filtration rate (GFR) both in the initial high renin phase of hypertension and later when plasma levels are normal. Angiotensin II also maintains GFR in less severe stenosis, which does not cause hypertension. This homeostatic action of angiotensin II to maintain GFr has minimal effects on blood flow. In renal-wrap hypertension, plasma renin levels are elevated for longer than after renal artery stenosis, but in other respects this initial phase of the hypertension is similar to that after renal artery stenosis. GFR is reduced, the rate of development of hypertension is accelerated by angiotensin II, and angiotensin II maintains the glomerular filtration fraction. Renal resistance is markedly increased owing to both compression of the kidney by the hypertrophying renal capsule and to angiotensin II. Thus angiotensin II apparently plays a primarily homeostatic role in renovascular hypertension to maintain glomerular ultrafiltration. It is suggested that the angiotensin II may be formed intrarenally and may act on sites other than resistance blood vessels.     

Humoral and neurogenic factors in two-kidney renovascular hypertension

A "bolus" dose (110 microgram) of the angiotesin II (A II)-blocker 1-Sar-8-Ala-A II (Saralasin, S) followed by its slow rate infusion (5 microgram/min/rat) for thirty min, was injected before and after the complete ganglionic blockade by pentolinium (P) in unanaesthetized unilaterally clipped renal hypertensive rats (the opposite kidney remained untouched). Pentolinium was also injected like a "bolus" dose (3 mg) followed by slow infusion (0.1 mg/min/rat) for thirty min. The observations were made until the fifth week after clipping the left renal artery. A consistent maximal hypotensive response was observed after the "bolus test" with both drugs. When S was the first drug injected, an inverse correlation was found between the percent decrease in arterial pressure (BP) by S and the percent decrease in BP by P (r = --0.83, P < 0.01, n = 8). Thus whenever a greater hypotensive effect was obtained by S, a smaller neural pressor component remained to be blocked by P. On the other hand, when P was the first drug injected a lesser A II pressor component remained to be blocked by S in the hypertensive rats. The results suggest that a considerable A II pressor effect in two-kidney renovascular hypertension is mediated via neurogenic mechanisms from the first week. A direct pressor vasoconstriction was found to be significant in cases with very high plasma-renin activity.     

Participation of the renin-angiotensin system in experimental renovascular hypertension

Hypertension was induced in Wistar rat by means of a clip in the left renal artery. After two weeks (acute stage) and sixteen weeks (chronic stage) the animals had a significant increase in arterial pressure (AP) and plasma renin activity (PRA). At both stages, nephrectomy or revascularization of the ischemic kidney returned AP and PRA to the normal level, both in the short term (1 day) and long term (60 days).     

The adrenal renal vascular connection plays an essential role in the pathogenesis of renovascular hypertension in the rat.

The adrenal renal portal circulation (ARPC) contributes to decrease in renal blood flow occurring after renal artery clipping. The aim of present study was to determine the role of the ARPC in the development of the renovascular hypertension in 1-kidney 1-clip model in the rat. Experiments were performed on male Wistar rats. In the control group (A) the right nephrectomy and adrenalectomy were done. In the experimental groups renovascular hypertension was produced by clipping the left renal artery (silver clip ID 0.40 mm). In the first of the experimental groups (B) the right nephrectomy and adrenalectomy were done. In the second experimental group (C), for elimination of the ARPC, the right kidney and the left adrenal gland were removed. In the half number of rats from each group plasma renin activity was measured 48 hours after surgery. An increase in SBP was significantly higher in the group B (ARPC intact) than in the group C (ARPC eliminated) (172 +/- 4 vs 144 +/- 2 mmHg, p.<0.01). PRA was significantly higher in the group C than in the group B (39.0 +/- 1.4 vs 31.2 +/- 2.0 mmol/l/min, p.<0.05). In the control group (A) PRA was significantly lower as compared to the both experimental group (2.0 +/- 1.6 mmol/l/min, p.<0.05).