Synthetic atrial natriuretic factor in conscious normotensive and hypertensive rats.

Seymour, A A; Marsh, E A; Mazack, E K; Stabilito, Inez I.; Blaine, Edward H.

doi:10.1161/01.hyp.7.3_pt_2.i35

Cited by 55 publications

(29 citation statements)

References 23 publications

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“…Such an interaction would be consistent with the observations that, compared with the responses in other hypertensive models, the natriuretic responses 9 and the depressor responses 10 to acute administration of ANP were exaggerated in two-kidney, one-clip hypertensive rats, a model in which renin levels are elevated.…”

supporting

confidence: 87%

Renal effects of atrial natriuretic factor during control of the renin-angiotensin system in anesthetized dogs.

Seymour

Mazack

1988

Circulation Research

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The contribution of the renin-angiotensin system to the natriuretic responses to intrarenal infusions of 1, 5, 25, and 125 pmol/kg/min synthetic rat atrial natriuretic peptide 101-126 was determined in one-kidney anesthetized dogs. In vehicle-treated dogs, atrial natriuretic peptide 101-126 increased fractional sodium excretion from 1.8 ±0.6% to a peak response of 5.1 ±0.9% during infusion of 25 pmol/kg/min. The peptide progressively decreased mean arterial pressure from 110±5to94±4 mm Hg, renal vascular resistance from 0.40 ± 0.02 to 0.30 ± 0.02 mm Hg/ml/min, and arterial plasma renin activity from 4.3 ±1.6 to 3.1 ±0.8 ng/ml/hr. When the renin-angiotensin system was blocked by 3 mg/kg i.v. enalaprilat, baseline pressure fell to 86 ±4 mm Hg, and subsequent infusions of atrial natriuretic peptide 101-126 did not affect fractional sodium excretion. The decreases in blood pressure N umerous studies have demonstrated that atrial natriuretic peptides (ANP) increase sodium excretion, lower mean arterial pressure (MAP), and suppress the renin-angiotensin system in both conscious and anesthetized dogs.1 " 7 Since angiotensin II (ang II) produces vasoconstriction and enhances sodium reabsorption, 8 the depressor and natriuretic effects of ANP may be due in part to the reduction in endogenous renin levels. Such an interaction would be consistent with the observations that, compared with the responses in other hypertensive models, the natriuretic responses 9 and the depressor responses 10 to acute administration of ANP were exaggerated in two-kidney, one-clip hypertensive rats, a model in which renin levels are elevated.In the present study, the renal and systemic responses to intrarenal administration of synthetic rat ANP 101-126 were determined before and after interruption of the renin-angiotensin system by inhibition of angiotensin converting enzyme (ACE) with the acid form of enalapril, MK 422 (enalaprilat), in anesthetized dogs. After ACE inhibition, ang II levels were increased by intravenous infusion of that peptide at a dose that restored blood pressure to control levels. Since intra- venous ang II elevated both renal perfusion pressure and renal vascular resistance, a second group of dogs was studied in which the vasoconstrictor effects of ang II were restricted to the kidney by intrarenal artery infusion of ang II. The responses to ANP 101-126 measured during intrarenal and intravenous ang II administration were compared with those obtained during intrarenal and intravenous infusions of the a-adrenergic agonist, methoxamine (ME). In this way, the contribution of the renin cascade to the biological effects of ANP 101-126 was determined. Materials and MethodsEighteen female mongrel dogs were anesthetized with vinbarbital (50 mg/kg i.v.) and intubated with a cuffed endotracheal tube. Ventilation with room air was maintained by a respirator (Harvard, South Natick, Massachusetts). Each animal was supported in an upright position, and both kidneys were exposed via bilateral flank incisions. Following unilateral nephre...

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confidence: 87%

Renal effects of atrial natriuretic factor during control of the renin-angiotensin system in anesthetized dogs.

Seymour

Mazack

1988

Circulation Research

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“…In another study in rats, however, an exaggerated blood pressure response to ANF was found during mineralocorticoid escape. 28 Since we found no consistent effect on effective renal plasma flow during ANF infusion, whether given before or during mineralocorticoid escape, an effect of escape on the vascular response to ANF was not apparent in our study.…”

Section: Discussioncontrasting

confidence: 62%

Enhanced natriuretic effect of atrial natriuretic factor during mineralocorticoid escape in humans.

Gaillard¹,

Koomans²,

Rabelink³

et al. 1988

Hypertension

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SUMMARY We examined the question of whether escape from the sodium-retaining effect of mineralocorticoid involves an increased natriuretic effect of atrial natriuretic factor (ANF). Seven healthy volunteers taking a 170 mmol Na/100 mmol K diet received an intravenous bolus (25 /xg) followed by a 1-hour infusion (0.02 /ig/kg/mln) of ANF (human ANF-[99-126]) before and after 10 days of 9-fludrocortisone acetate, 0.5 mg b.i.d. Escape was accompanied by an increase in body weight (from 72.2 ± 12.9 to 74.0 ± 12.6 kg; p < 0.05), mean arterial pressure (from 95 ± 4 to 109 ± 3 mm Hg; p < 0.01), plasma ANF (from 9 ± 2 to 24 ± 4 pmol/L; p < 0.01), and Inulin clearance (from 124 ± 9 to 137 ± 7 ml/min; p < 0.05). Indexes for renal sodium handling (lithium and free water clearance) were compatible with a decreased "proximal" and an Increased "distal" tubular reabsorption fraction. ANF Infusion raised inulin clearance comparably before and after escape to 138 ± 10 and 152 ± 7 ml/min, respectively, but the natriuretic effect was much larger (p < 0.05) after escape (from 366 ± 34 to 1294 ± 278 pmol/ min) than before (from 248 ± 48 to 630 ± Y2A /unol/min). Indexes for tubular reabsorption were consistent with greater suppression of both "proximal" and "distal" tubular sodium reabsorption by ANF after versus before mineralocorticoid expansion. These results indicate that escape is accompanied not only by a rise in plasma ANF but also by potentiation of the natriuretic effect of ANF. This effect involves enhanced suppression of tubular sodium reabsorption rather than enhanced elevation of filtered load. Elevated blood pressure, and thus renal perfusion pressure, may be responsible for this effect.

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“…These observations agree with results for other forms of chronic hypertension. For example, similar responses to ANF have been observed in Dahl saltsensitive, 19 deoxycorticosterone acetate-salt, 18 and one-kidney, one clip 31 hypertensive rats and their normotensive controls.…”

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confidence: 61%

Exaggerated natriuretic response to atrial natriuretic factor in rats developing spontaneous hypertension.

Pollock

Arendshorst

1990

Hypertension

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The present study was designed to evaluate the renal response to atrial natriuretic factor (ANF) in young rats developing spontaneous hypertension (SHR) and compare this response to age-matched, normotensive controls (WKY) and adult animals. At 6 weeks of age, intravenous infusion of ANF (0.25 /tg/kg min) in anesthetized, euvolemic rats produced a significantly larger natriuresis and diuresis in SHR compared with WKY rats; this strain difference was not observed in rats 11 weeks of age. SHR showed no age-related change in the natriuretic response to ANF, whereas adult WKY rats exhibited a greater response than young WKY rats. To determine the effect of renal perfusion pressure on the magnitude of the renal response to ANF, additional groups of 6-and 11-week-old SHR were studied while renal perfusion pressure was lowered acutely by aortic constriction (SHR-AC) to values similar to age-matched WKY rats. In young rats, the diuretic and natriuretic response to ANF was greatest in SHR, intermediate in SHR-AC, and lowest in WKY rats. In adult animals, the natriuretic and diuretic response was similar in SHR and WKY rats and tended to be less in SHR-AC. These results in both 6-and 11-week-old SHR are consistent with previous reports that the magnitude of the response to ANF is directly related to acute changes in renal perfusion pressure. Furthermore, we conclude that 1) the kidney of young SHR is hyperresponsive to ANF, 2) WKY rats, but not SHR, exhibit age-related increases in responsiveness to ANF, 3) increased renal perfusion pressure cannot completely account for the exaggerated renal response in young SHR, and 4) the relation between pressure and the response to ANF is not observed with chronic elevations in renal perfusion pressure in hypertensive rats. (Hypertension 1990;16:72-79)

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Synthetic atrial natriuretic factor in conscious normotensive and hypertensive rats.

Cited by 55 publications

References 23 publications

Renal effects of atrial natriuretic factor during control of the renin-angiotensin system in anesthetized dogs.

Renal effects of atrial natriuretic factor during control of the renin-angiotensin system in anesthetized dogs.

Enhanced natriuretic effect of atrial natriuretic factor during mineralocorticoid escape in humans.

Exaggerated natriuretic response to atrial natriuretic factor in rats developing spontaneous hypertension.

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