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Sodium Intake and Hypertension
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
T. O. Morgan, F. A. O. Mendelsohn, A. E. Doyle
There is also good evidence that in mineralocorticoid hypertension, the rise in blood pressure is secondary to sodium retention. Patients with primary aldosteronism characteristically have somewhat elevated serum sodium levels, hypokalemia, increased extracellular fluid volume, and a low plasma renin level.78 Similar changes occur in other varieties of mineralocorticoid hypertension, such as that associated with 17-hydroxy-iation deficiency79 or with excess production of 18-hydroxy-l 1-deoxycorticosterone.80 High doses of spironolactone cause reversal of these clinical manifestations, leading to a fall in serum sodium, a rise in serum potassium levels, a fall in extracellular fluid volume, together with a fall in blood pressure and a rise in plasma renin levels.81 These changes can also be induced by amiloride, suggesting that they are related to the effects on body sodium via distal tubular sodium excretion rather than to any other action of aldosterone. Moreover, dietary sodium restriction alone may occasionally induce a fall in blood pressure and body weight (Figure 16).
Hypertension and the Kidney
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Roberto Pontremoli, Giovanna Leoncini, Francesca Viazzi
The kidney as the long-term regulator of BP and fluid homeostasis. In the 1970s, Arthur Guyton and colleagues provided solid experimental and clinical evidence in support of the dominant role of the kidney in the regulation of BP through its long-term fine tuning of extracellular fluid volume. Building on the hypothesis that the maintenance of body fluid balance requires an accurate match between salt and water intake and output (14), Guyton elegantly showed that any increase in BP, independent of its cause, will eventually be reverted in the long run by the consequent increase in renal perfusion pressure, a phenomenon called pressure-natriuresis (Figure 3.1). This mechanism was proved to have sufficient gain to limit intravascular volume expansion and to lower blood pressure in response to a wide range of stimuli such as increase in heart rate or elevated peripheral vascular resistance (15,16). According to Guyton’s experimental work, a modification of the pressure-natriuresis response with a shift to a higher BP level is a prerequisite in order to produce a sustained, long-term BP elevation at the systemic level. However, more recent evidence points toward a more complex relationship between sodium retention and extracellular fluid volume homeostasis.
Dopamine And The Kidney
Published in M.D. Francesco Amenta, Peripheral Dopamine Pathophysiology, 2019
The natriuretic action of DA has proved to be beneficial in treatment of heart failure and renal failure, and may be useful in therapy of hypertensive and edematous states characterized by sodium retention. Defects in the pathways responsible for normal release of renal DA seem likely to be implicated in the etiology of a subpopulation of essential hypertensives in whom salt retention and volume expansion is present, and assessment of plasma or urinary DA levels, relative to those of NA, appears to provide an index for rapid identification of this population. As well, some syndromes characterized by reduced plasma volume and orthostatic or episodic hypotension may be explicable on the basis of excessive dopaminergic natriuresis.
Paeonol improves renal and vascular angiotensin II type 1 receptor function via inhibiting oxidative stress in spontaneously hypertensive rats
Published in Clinical and Experimental Hypertension, 2023
Tingchun Wu, Yuhua Zheng, Qianqian Huang, Shui Tian
Hypertension is an independent risk factor for cardiovascular and cerebrovascular diseases such as acute myocardial infarction, stroke, and heart failure (24,25). Since sodium retention and enhanced vasoconstriction are the hallmark of essential hypertension, a growing number of studies have focused on abnormal renal sodium handling and vasoconstriction in the pathogenesis of hypertension (26,27). AT1R, as an important component of RAS, is an important regulator of sodium homeostasis, vasoconstriction and relaxation, and blood pressure (28). We showed a causal link between oxidative stress and renal and vascular AT1R function, because antioxidant paeonol treatment restored renal and vascular AT1R function and reduced blood pressure in SHRs. The objective of the current study was to investigate the biochemical mechanisms by which paeonol treatment may reduce oxidative stress, alter renal and vascular AT1R function, leading to a decrease in blood pressure in SHRs.
The pharmacotherapeutic options in patients with catecholamine-resistant vasodilatory shock
Published in Expert Review of Clinical Pharmacology, 2022
Timothy E. Albertson, James A. Chenoweth, Justin C. Lewis, Janelle V. Pugashetti, Christian E. Sandrock, Brian M. Morrissey
When either NE or AT-II were infused over a prolonged period in seven normal and eleven patients with cirrhosis, different effects were seen between the two drugs and the two populations [73]. Normal subjects demonstrated initial pressor response to NE with transient natriuresis for 2–4 days and followed by diminished vasopressor responsiveness. Cirrhosis patients showed transient natriuresis and diuresis with reduced vasopressor responsiveness to NE but tachyphylaxis was minimal. The infusion of AT-II in normal subjects initially resulted in sodium retention and increased vasopressor effects. After 3–5 days, reduced retention of sodium was seen, and weights stabilized. The AT-II infusions resulted in increased aldosterone levels without increased cortisol levels. Sodium-depleted normal subjects failed to demonstrate sodium retention and had reduced vasopressor effects [73]. The cirrhosis patients infused with AT-II produced striking natriuresis and diuresis with reduction of peripheral edema. In addition, vasopressor unresponsiveness and tachyphylaxis were seen in those that did respond to AT-II. These early studies demonstrate important non-vasopressor effects of AT-II and a disease–drug interaction.
An overview of alogliptin + pioglitazone for the treatment of type 2 diabetes
Published in Expert Opinion on Pharmacotherapy, 2022
Brian Tomlinson, Paul Chan, Christopher Wai Kei Lam
Pioglitazone causes a dose-related increase in body weight which is partly due to fat deposition in subcutaneous fat stores while there is reduction in visceral fat and other sites of ectopic fat deposition [56]. It also increases total body fluid, which accounted for 75% of the weight gain in one study [117]. Despite the increase in total body sodium, blood pressure is usually reduced, and peripheral vasodilatation may contribute to the sodium retention [118]. The volume retention appears to be related to alteration of sodium handling by activation of PPAR-γ receptors in the endothelial cells lining the renal collecting duct [119]. Increased expression of epithelial sodium channels appears to be involved [120]. Fluid retention with pioglitazone is dose-related and is greater when used in combination with a sulfonylurea or insulin [121,122].