Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphometrical investigations (point-counting method) showed that in different inflammatory (endocapillary -- acute -- GN, mesangioproliferative GN, membranoproliferative GN) glomerulonephritides and in non-inflammatory glomerular diseases (perireticular amyloidosis), there are statistically significant correlation between serum creatine concentrations at the time of biopsy and the enlargement of the cortical interstitium by fibrosis. Similar results were obtained in investigating different grades of benign nephrosclerosis with transition into secondary malignant nephrosclerosis conditioned by hypertension and in chronic diffuse sclerosing interstitial nephritides of different etiologies. As hypothesis, we assume that a narrowing of the postglomerular vessel network by interstitial fibrosis take place. This could lead to an increase resistance of the renal cortical blood flow. In spite of an elevated effective filtration pressure, the slowing of the glomerular blood flow may lead to the reduction of GRF and to an increase of the serum creatinine concentration. Additionally, in the case of interstitial fibrosis the tubules look atrophied. This could be the consequence of the reduced GFR as a sign of inactivity. On the other hand, tubular atrophy could result from malnutrition in the case of interstitial fibrosis. The resorptive capacity of these atrophied-looking tubules could be lowered and the GFR could be diminished by the so-called Thurau mechanism.
 ...
PMID:The role of the interstitium of the renal cortex in renal disease. 46 60

A new method was developed for separate kidney function studies by catheterizing the ureters and exteriorizing the catheters through the urethra into the vagina. Renal artery plication was performed to reduce blood flow to one kidney by 66 +/- 5%. Arterial pressure increased from 107 +/- 2 to 131 +/- 3 mmHg and remained elevated for 28 days. Plasma renin activity was increased for the first 7-10 days only. Sodium and water excretion were markedly reduced in the kidney with the stenosed renal artery and after the first 2 days Na and water excretion were incresed in the contralateral kidney. These changes in Na and water excretion were frequently associated with similar directional changes in glomerular filtration rate (GFR) and renal plasma flow. An exception was noted in that renal sodium and water excretion remained low throughout the 28 days in the kidney with the constricted renal artery, whereas GRF returned to near the control level by the end of 2 wk. Altered filtration fraction did not appear to be a determining factor in control of the rate of Na excretion. It is suggested that GFR, the renin-angiotensin-aldosterone system, and other as yet undefined factors are involved in salt and water homeostasis during unilateral renal artery stenosis with hypertension.
 ...
PMID:Separate renal function studies in conscious dogs with renovascular hypertension. 69 70

Acute dissection of the aorta is a rare disease which, when left untreated, has a disastrous prognosis. Two aetiological factors are essential: acquired or congenital fragility of the aortic elastic tissue, and arterial hypertension. The condition must be diagnosed as early as possible to avoid a fatal outcome: it is a surgical emergency. The clinical diagnosis rests on a history of migrating pain and on the presence of signs of ischaemia in a vascular territory. It is confirmed by complementary investigations, chiefly angiography. Acute dissection of the ascending aorta is treated by surgery: the ascending segment is resected, the distal cylindres are recoupled to close the portal of entry, and the aortic regurgitation is treated by valvuloplasty or aortic valve replacement. The introduction of the GRF biological glue has considerably improved the per-operative prognosis and lowered the hospital mortality to 10%. Long-term post-operative follow-up of the patient is crucial, since iterative dissection and formation of aneurysms are not exceptional, especially in patients with Marfan's syndrome.
 ...
PMID:[Acute dissection of the aorta in 1986. Proposal for a new anatomopathological classification]. 294 2

The relationship between the fractional excretion of filtered sodium (FENa) and the peritubular capillary physical factors (PCPF) in the hypertension (HT) of chronic glomerulonephritis (GN) was examined in hydropenia (C) and during sustained isotonic saline volume expansion (E; 3% net increase of body weight) in 32 GN patients (16 with HT), and compared with our previous findings in 20 normal individuals (NORM) and 19 patients with essential hypertension (EH). Fourteen GN patients (seven with HT) had a 75% reduction of glomerular filtration rate (GFR), the others (nine with HT) had normal or near normal GFR. The PCPF were estimated from the intrarenal venous (wedged) pressure (IRVP) and the calculated efferent arteriolar protein concentration (EAPC). In C, IRVP correlated to GFR (r = 0.682, p less than 0.001) and (FENa) (r = -0.357, p less than 0.05), but IRVP and EAPC were similar in HT and normotension at comparable levels of GFR. The increase of FENa during E (delta FENa) was exaggerated in all HT groups even at reduced levels of GRF, and could not be related to changes in renal hemodynamics or PCPF. delta FENa correlated with mean arterial pressure in C both in GN (r1 = 0.702, p less than 0.01) and in the combined NORM/EH group (r2 = 0.478, p less than 0.01), with r1 greater than r2 (p less than 0.005). The findings indicate that the pathogenesis of hypertension of chronic glomerulonephritis is independent of changes in the PCPF, and are compatible with the idea that humoral factors are the main mediators of the altered sodium excretion during saline volume expansion in the HT of both chronic GN and EH.
Hypertension
PMID:Intrarenal pressure and sodium excretion in hypertension of chronic glomerulonephritis in humans. 684 Aug 24

CS-905 is a dihydropyridine calcium channel antagonist which stands out for its prolonged hypotensive effect, and which is currently under investigation for the treatment of hypertension. The aim of the current series of studies was to investigate the effects of CS-905 on renal function in relation to its effects on arterial pressure. In anesthetized spontaneously hypertensive rats (SHR), intravenous bolus injection of CS-905 reduced mean arterial pressure (MAP) in a dose-dependent fashion. In parallel, there was a dose-related increase in urine flow (V), sodium excretion (UNaV), renal plasma flow (RPF), and glomerular filtration rate (GFR). In chronically cannulated unanesthetized SHR, single-dose CS-905 by gavage produced a sustained reduction in MAP, a significant increase in V and UNaV, no effect on RPF, and an increase in GFR. Continuous intrarenal infusion of CS-905 in anesthetized normotensive Munich Wistar rats at doses that did not affect MAP caused a marked diuresis and natriuresis, without affecting RPF or GFR. To determine whether the diuretic and natriuretic effects of CS-905 were mediated by changes in inner medullary blood flow, the effect of CS-905 on vasa recta blood flow (Qvr) was studied by fluorescent videomicroscopy in anesthetized normotensive Munich Wistar rats during continuous intrarenal infusion. At low infusion rates, CS-905 was diuretic and natriuretic while increasing Qvr. With a high infusion rate, although the diuretic and natriuretic effects of CS-905 were maximal, Qvr decreased. These findings suggest that the diuretic and natriuretic effects of CS-905 are dissociated from and cannot be accounted for by changes in RPF, GRF, or Qvr, and are most likely secondary to a direct action of CS-905 on renal tubule handling of sodium and water.
 ...
PMID:Effects of CS-905, a novel dihydropyridine calcium channel blocker, on arterial pressure, renal excretory function, and inner medullary blood flow in the rat. 794 66

Diuretic therapy is a drug therapy that increases urine volume, but not glomerular filtration rate (GFR). The diuretics act predominantly on tubular sites; the drugs that increase GRF are the aminophyllines, the positive inotropy or vasoactive substances that increase afferent arteriolar flux or intraglomerular pressure. We can divide the diuretics into six categories: 1) carbonic anhydrase inhibitors: acetazolamide, dichlorphenamide, methazolamide; 2) osmotic diuretics: glycerol, mannitol, urea; 3) loop diuretics: furosemide, bumetanide, ethacrynic acid, piretanide, torsemide; 4) thiazide and thiazide-like diuretics: chlorothiazide, trichlormethiazide, indapamide, chlorthalidone, metolazone; 5) potassium-sparers: a) kidney epithelial sodium channel inhibitors: amiloride and triamterene; b) aldosterone receptor antagonists: spironolactone, canrenoate potassium, eplerenone; 6) ADH antagonists: lithium salts, demeclocycline and ethanol. Diuretic therapy is useful in treating acute and chronic renal insufficiency, congestive heart failure, cirrhosis, overhydration and hypertension. Diuretic therapy increases urine volume, ion loss (except Na+, K+), and modifies diffusion (dilute urine) and convection mechanisms (reduced tubular absorption). Therefore, diuretics are very useful non-dangerous drugs.
 ...
PMID:[Diuretic therapy in heart failure]. 1663 1