Pathogenesis Of Hypertension In Patients Research Articles

Relationships Among Plasma Aldosterone, High-Density Lipoprotein Cholesterol, and Insulin in Humans

To investigate the pathogenesis of hypertension in patients with obesity and insulin resistance and to explore the role of plasma lipids, we studied 30 subjects at the end of 7 days of low (20 mEq/d) then high (200 mEq/d) sodium diets. Glucose and insulin tolerance tests were performed at the end of each week and blood and urine collected for measurements of plasma aldosterone, renin activity, electrolytes, insulin, and lipoproteins. There was a strong negative correlation between plasma aldosterone and high-density lipoprotein cholesterol during both diets. There were weaker positive correlations between plasma aldosterone and insulin or triglycerides. When the aldosterone-renin ratio was the dependent variable and the correlation controlled for serum potassium, the inverse relationship with high-density lipoprotein cholesterol and the positive correlation with insulin remained, but only during the high salt diet. Subjects were divided into three groups based on high-density lipoprotein cholesterol. Subjects with the lowest high-density lipoprotein cholesterol levels showed the highest aldosterone, plasma triglycerides, body mass index, and waist-to-hip ratio. Those subjects also demonstrated the greatest resistance to insulin action on glucose and plasma unesterified fatty acids. There was a weak direct correlation between plasma aldosterone and systolic blood pressure during the high salt diet. These data suggest that high aldosterone levels may be a link between dyslipidemia, insulin resistance, and hypertension, a relationship made more evident by high salt intake.

The role of endothelial factors, cyclosporine, and erythropoietin in hypertension in chronic renal failure

Hypertension is commonly observed in patients with renal insufficiency. The pathogenesis of this condition is multifactorial and not clearly understood. Recently, a great deal of attention has been paid to the role of endothelial factors, such as endothelin and endothelial-derived relaxing factor, in the regulation of the microcirculation and in the pathogenesis of hypertension. The role of these factors in the pathogenesis of hypertension in patients with renal insufficiency is reviewed. In addition, cyclosporine and erythropoietin have recently been used to prevent rejection in renal transplant patients and to treat anemia in patients with renal insufficiency. We review the evidence that these agents may cause or aggravate hypertension in patients with renal failure.

Reversible Renal Failure Associated with Angiotensin-Converting Enzyme Inhibitors in Polycystic Kidney Disease

The renin-angiotensin-aldosterone system appears to play an important initiating role in the pathogenesis of hypertension in patients with autosomal-dominant polycystic kidney disease (ADPKD). Therefore, angiotensin-converting enzyme (ACE) inhibitors would appear to be appropriate therapy for hypertension in such patients. However, because ADPKD is a bilateral disorder, ACE-inhibitor therapy may worsen renal function, as occurs in patients with bilateral renal artery stenosis. We describe eight episodes of reversible acute renal deterioration in five patients with ADPKD, massive renal involvement, and chronic renal insufficiency. In all cases, ACE-inhibitor therapy either predisposed the patient to or precipitated the acute event. Two of the patients who had acute renal failure while receiving ACE-inhibitor therapy experienced a recurrence when rechallenged with such therapy. Furthermore, patients receiving combined therapy with an ACE inhibitor and a diuretic and patients who experience a cyst hemorrhage while receiving ACE inhibitor therapy are also at risk for reversible renal dysfunction. Caution is therefore recommended in using ACE inhibitors to treat hypertension in patients with ADPKD who are at high risk because of compromised renal function and massive cystic involvement.

Role of type IV collagen (CIV) in the pathogenesis of portal hypertension in patients with alcoholic cirrhosis

Role of type IV collagen (CIV) in the pathogenesis of portal hypertension in patients with alcoholic cirrhosis

Role of endogenous serotonin in the regulation of blood pressure in patients with chronic renal failure.

Although the pathogenesis of hypertension in patients on maintenance haemodialysis is not completely understood, one of the important contributing factors is an increase in total peripheral vascular resistance (Kim et al. 1972). Page and McCubbin (1953) discovered the monoamine serotonin and suggested it may have a role in the regulation of blood pressure. However, its function in the regulation of blood pressure is still unclear. Clinical investigations of the serotonin S2-receptor antagonist ketanserin have shown that ketanserin reduces systemic vascular resistance and lowers blood pressure following acute or long term administration in patients with essential hypertension (De Cree et al. 1981; Fagard et al. 1984; Wenting et al. 1984). In this study, the acute effects of ketanserin on blood pressure and hormonal responses in 10 patients on maintenance haemodialysis with hypertension were determined in order to assess the role of endogenous serotonin in the regulation of blood pressure in such patients. The long term effect of ketanserin on pressor responsiveness to the £x,-adrenoreceptor agonist phenylephrine was also determined in 5 patients. 1. Methods

Blood pressure regulation, peripheral renin activity and aldosterone in patients with pyelonephritic renal scarring.

Patients with renal scarring due to previous upper urinary tract infections (UTI) are at risk of developing hypertension and renal insufficiency. In this study glomerular filtration rate (GFR), systolic (SBP) and diastolic (DBP) blood pressure, peripheral renin activity (PRA), plasma (p-Aldo) and urine aldosterone (u-Aldo), the urinary excretion of sodium (UNa) and potassium (UK) and the fractional sodium (CNa/CIn) and potassium (CK/CIn) excretion were determined in 22 female patients with verified renal scarring and a history of febrile UTI and in nine age-matched healthy women with normal i.v. urograms. The patients had significantly lower GFR, higher SBP, higher PRA and higher CK/CIn than the healthy controls. A significant correlation between CNa/CIn and SBP (r = 0.51, P less than 0.05), DBP (r = 0.50, P less than 0.05) and PRA (r = -0.47, P less than 0.05) was found. The ratio of UK/UNa was significantly correlated to SBP (r = -0.43, P less than 0.05), DBP (r = -0.44, P less than 0.05), PRA (r = 0.65, P less than 0.01) and p-Aldo (r = 0.68, P less than 0.01). It is concluded that the renin-aldosterone system probably is involved in the pathogenesis of hypertension in patients with pyelonephritic renal scarring and that screening determinations of UNa and UK may prove useful for detection of individuals with increased PRA and p-Aldo.

A Circulating Na+-K+ATPase Inhibitor, Erythrocyte Sodium Transport and Hypertension in Patients with Chronic Renal Failure

The level of circulating Na+-K+ATPase inhibitor (% inhibition), erythrocyte ouabain-sensitive 22Na+ efflux rate constant (Kos) and erythrocyte sodium content (RBC Na) were measured in 11 undialysed patients with chronic renal failure, 16 patients on chronic hemodialysis and 16 age-matched normotensive healthy controls. In uremics, % inhibition was significantly higher than that in the controls (p less than 0.001). There were significant correlations between % inhibition and both mean blood pressure (r = 0.74, p less than 0.001) and Kos (r = -0.47, p less than 0.005) for all the groups combined. Hypertensive uremics showed significantly higher % inhibition, lower Kos and higher RBC Na compared with normotensive ones. These data suggest that the elevated level of circulating Na+-K+ ATPase inhibitor may, at least in part, account for the pathogenesis of hypertension in patients with chronic renal failure.