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PubMed1995

Pressure natriuresis and long-term blood pressure control.

The relationship between arterial pressure and the rate of Na+ excretion is regulated by a number of mechanisms- some well known, some newly discovered, and probably some yet to be discovered. These mechanisms affect either the amount of Na+ filtered at the glomerulus or its rate of reabsorption from the proximal or distal tubule. Other than physical factors (plasma protein concentration, glomerular capillary and tubular pressures) and glomerular ultrafiltration properties (Kr), important regulators of both filtration and reabsorption include the renin-angiotensin system, aldosterone, and renal nerves, although much remains to be learned about renal sympathetic innervation, especially neural control of renal tubular function. It has recently become evident that other factors may also be important, in particular, nitric oxide, endothelin, and medullipin. The latter is a vasodepressor hormone released from the renal medulla by increased arterial pressure, and its role in pressure-related Na+ excretion is only now being studied. Despite the central importance of this mechanism in the regulation of arterial pressure, there has been little study of many other potentially important mechanisms, especially those capable of affecting active Na+ transport across the tubule, including the imidazoline-preferring receptors. New techniques to study the relationship between arterial pressure and Na+ excretion are becoming available, and these will allow a better assessment of the potential of pharmacologic agents capable of modifying this relationship.

Animals↗
PubMed1995

Renal I1-imidazoline receptor-selective compounds mediate natriuresis in the rat.

In the present study, we investigated the renal actions of two compounds reported to interact with the imidazoline receptor: rilmenidine (I1-receptor selective, centrally acting antihypertensive) and agmatine (an endogenous clonidine-displacing substance). Rilmenidine (saline vehicle, 3 or 30 nmol/kg/min) or agmatine (saline vehicle, 3 or 30 nmol/kg/min) was infused directly into the renal artery of anesthetized (pentobarbitone) Sprague-Dawley rats (280-300 g) that had undergone a unilateral nephrectomy 7 to 10 days before the experiment. Rilmenidine produced an increase in urine flow rate at doses that failed to significantly alter blood pressure, creatinine clearance, or heart rate. The increase in urine flow rate was secondary to an increase in osmolar clearance, primarily composed of sodium. Free water clearance was not altered at these infusion rates. Agmatine also increased urine flow rate at doses that failed to alter blood pressure, creatinine clearance, and heart rate. The increase in urine flow rate was secondary to an increase in osmolar clearance, again primarily composed of sodium. The natriuretic action of rilmenidine and agmatine, at doses that do not lower blood pressure acutely, could be beneficial in the antihypertensive actions of these centrally acting agents.

Adrenergic alpha-Agonists↗
PubMed1996

The lysine-1 analog of guanylin induces intestinal secretion and natriuresis in the isolated perfused kidney.

Guanylin is an endogenous peptide synthesized by several mammalian species that mimics the effects of a thermostable enterotoxin of Escherichia coli (STa: NTFYCCELCCNPACAGCY) in the gut. We have cloned a lysine-1 derivative of rat guanylin (Lys-1-NTCEICAYAACTGC) and tested its effects on ileal tissue membranes in Ussing chambers and in the isolated perfused rat kidney. Rabbit ileal mucosa membranes were mounted into a Ussing chamber and the effects of Lys-1 guanylin (Lys-1 G) and STa enterotoxin peptide on chloride secretion were determined by changes in short-circuit current (Isc). Lys-1 G (10 to 100 nM) showed a dose-dependent effect on chloride secretion with a maximal response estimated to be 52 microA/cm2. Lys-1 G mimics the effect of STa peptide, but the enterotoxin elicited a greater maximal effect of 120 microA/cm2 (P < 0.01). Lys-1 G (2.5 micrograms/ml) promoted an increase in both urine flow (from 0.13 +/- 0.07 to 0.40 +/- 0.01 ml g-1 min-1, N = 4; P < 0.05) and glomerular filtration rate (from 0.68 +/- 0.02 to 0.85 +/- 0.00 ml g-1 min-1, N = 4; P < 0.01) in the isolated perfused kidney and a reduction of the fractional reabsorption of sodium (from 76.0 +/- 0.03 to 59.5 +/- 0.85%, N = 4; P < 0.01). These maximal effects were accompanied by intense natriuretic effect observed 30 and 60 min after drug administration. The Lys-1 G analog similar to STa enterotoxin elicited intestinal chloride secretion and a natriuretic effect. These data demonstrate that the cloned peptide analog retains the biological activity of the native hormone and presents activity similar to STa. The properties of Lys-1 G resemble those of a factor formed during perfusion of the hypoxic rabbit kidney and named by us factor natriureticus similis (FNS).

Animals↗
PubMed1988

The effect of fludrocortisone acetate on plasma volume and natriuresis in patients with aneurysmal subarachnoid hemorrhage.

In order to prevent hypovolemia fludrocortisone acetate treatment was started on admission in 39 consecutive patients with CT evidence of subarachnoid hemorrhage. In 28 patients an aneurysm was proven or probable, and in 21 of these the effects of fludrocortisone acetate on sodium balance and on plasma volume could be studied. In the first five days plasma volume decreased more than 10% in four patients, decreased less than 10% in five and increased in 12. The cumulative sodium balance measured over five days was negative in seven of the 21 patients. Plasma renin values were measured in 15 of the 21 patients and also in stored samples of 18 patients who were not treated with fludrocortisone acetate. Plasma renin values were less high in patients treated with fludrocortisone acetate, regardless of the presence of a negative sodium balance. In three of the 39 patients signs of pulmonary edema developed, and low serum potassium values were observed in four of the 21 patients. In comparison with previous studies, these findings suggest that fludrocortisone acetate is an effective method of decreasing the incidence of volume depletion and negative sodium balance.

Blood Volume↗
PubMed1976

Natriuresis induced by intracarotid infusion of hypertonic NaCl.

The intracarotid infusion of hypertonic sodium chloride in anesthetized dogs pretreated with vasopressin and mineralocorticoid resulted in an increase in sodium excretion as well as an increase in the percent of the filtered load of sodium excreted. This increase was not due to changes in renal hemodynamics or arterial blood pressure. The change in fractional sodium excretion was approximately 1%. Intracarotid infusion of isotonic sodium chloride did not result in a natriuretic response. The intracarotid infusion of hyperosmotic glucose did not evoke an increase in sodium excretion. Femoral vein infusions of hypertonic sodium chloride failed to evoke any natriuretic response. These data indicate that a sodium-sensing mechanism may exist in the brain that can alter the renal handling of sodium. The efferent mechanism of the response is discussed.

Animals↗
PubMed1983

Hemodynamic mechanisms in CNS-induced natriuresis in the conscious rat.

These experiments were designed to determine 1) the effects of increased CSF sodium concentration on renal hemodynamics in the conscious rat, and 2) the role of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) in the natriuretic and hemodynamic responses during this treatment. After electrolytic lesions of AV3V periventricular tissue or control surgery, blood pressure, glomerular filtration rate, effective renal blood flow, urine volume, and sodium and potassium excretion were measured before and during intraventricular (IVT) infusion of either isotonic or hypertonic saline solutions in conscious hydrated rats. Blood pressure, glomerular filtration rate, and sodium and potassium excretion increased during IVT infusion of concentrated sodium solutions in control rats but not in animals with lesions in the AV3V region. These data support the hypothesis that the natriuretic response to increased CSF sodium concentration in the rat is due to a pressor response and/or increased glomerular filtration rate and demonstrate that ablation of AV3V periventricular tissue blunts the natriuretic response, possibly through diminished central pressor mechanisms and/or decreased central control of glomerular filtration rate.

Animals↗
PubMedDate not supplied

The 'body fluid pressure control system' relies on the Renin-Angiotensin-aldosterone system: balance studies in freely moving dogs.

1. The physiological role of the 'renal body fluid pressure control system', including the intrarenal mechanism of 'pressure natriuresis', is uncertain. 2. Balance studies in freely moving dogs address the following questions: (i) what is the physiological contribution of pressure natriuresis to the control of total body sodium (TBS); (ii) to what extent is long-term mean arterial blood pressure (MABP) determined by TBS and total body water (TBW); and (iii) during Na accumulation, is Na stored in an osmotically inactive form? 3. Diurnal time-courses of Na excretion (U(Na)V) and MABP reveal no correlation. Spontaneous MABP changes do not affect U(Na)V. The long-term 20% reduction of renal perfusion pressure (RPP) results in Na retention via pressure-dependent stimulation of the renin-angiotensin-aldosterone system (RAAS), not via a pressure natriuresis mechanism. Prevention of pressure natriuresis does not result in ongoing Na retention when the RAAS is operative. The long-term 20% elevation of RPP induced by sustained TBS elevation facilitates Na excretion via pressure natriuresis, but does not restore TBS to normal. 4. Changes in TBW correlate well with changes in TBS (r(2) = 0.79). This correlation is even closer when concomitant changes in total body potassium are also considered (r(2) = 0.91). 5. With normal or elevated TBW, long-term MABP changes correlate well with TBW changes (r(2) = 0.69). At lowered TBW, no correlation is found. 6. In conclusion, the physiological role of pressure natriuresis is limited. Pressure natriuresis does not appear to be operative when RPP is changed from -20 to +10% and neurohumoral control of U(Na)V is unimpeded. Within this range, pressure-dependent changes in the RAAS mediate the effects of changes in RPP on U(Na)V. Pressure natriuresis may constitute a compensating mechanism under pathophysiological conditions of substantial elevation of RPP. A large portion of the long-term changes in MABP are attributable to changes in TBW. The notion of osmotically inactive Na storage during Na accumulation appears to be invalid.

Animals↗