The mechanisms responsible for increased total peripheral resistance (TPR) during high salt intake in salt-sensitive subjects are not fully understood but likely involve pressure-dependent and/or flow-dependent autoregulation in peripheral tissues as well as neurohormonal factors that occur concomitantly with kidney dysfunction.

2016年3月1日 · In this review, I discuss evidence that kidney dysfunction is required for chronic increases in BP in subjects who are salt sensitive and that vasoconstriction of nonrenal blood vessels, although present in salt-induced hypertension, is insufficient to chronically increase BP in the absence of kidney dysfunction.

Salt retention as a result of chronic, excessive dietary salt intake, is widely accepted as one of the most common causes of hypertension. In a small minority of cases, enhanced Na + reabsorption by the kidney can be traced to specific genetic defects of salt transport, or pathological conditions of the kidney, adrenal cortex, or pituitary.

2017年4月1日 · Salt sensitivity, associated with inability of ANG II to respond to changes in salt intake, occurred with smaller changes in renal blood flow but greater changes in glomerular filtration rate, renal sodium reabsorption, and total peripheral resistance (TPR). However, clamping TPR at normal or high levels had no major effect on salt sensitivity.

2016年5月9日 · Within this theoretical framework, later increases in TPR occur as an autoregulatory response to tissue hyperperfusion. Increased TPR maintains or exaggerates the BP elevation and resets CO back to normal, via pressure natriuresis. Three types of observations render support for this theory.

Total peripheral vascular resistance (TPR) may initially decrease, perhaps as a result of reflex/hormonal mecha-nisms that cause vasodilation in response to volume load-ing, but within a few days, TPR returns to nearly normal as salt/volume balance is re-established and CO and BP return to nearly normal levels. In salt-sensitive subjects, high salt

Thirty-four elderly patients were studied using a Doppler flowmeter during different sodium intakes. Salt increased mean blood pressure and cardiac output (CO), while total peripheral resistance (TPR) remained unchanged.

Office BP, ABPM, augmentation index (AI x), pulse wave velocity (PWV), cardiac output (CO), and total peripheral resistance (TPR) were automatically measured. Estimation of salt intake was assessed by 24‐hour urinary sodium excretion.

2016年3月1日 · The mechanisms responsible for increased total peripheral resistance (TPR) during high salt intake in salt-sensitive subjects are not fully understood but likely involve pressure-dependent and/or flow-dependent autoregulation in peripheral tissues as well as neurohormonal factors that occur concomitantly with kidney dysfunction.

2017年4月1日 · Salt sensitivity, associated with inability of ANG II to respond to changes in salt intake, occurred with smaller changes in renal blood flow but greater changes in glomerular filtration rate, renal sodium reabsorption, and total peripheral resistance (TPR). However, clamping TPR at normal or high levels had no major effect on salt sensitivity.