Renal and blood pressure responses to synthetic atrial natriuretic factor in spontaneously hypertensive rats.

Marsh, E A; Seymour, A A; Haley, Anne B.; Whinnery, M. A.; Napier, Mary E.; Nutt, Ruth F.; Blaine, Edward H.

doi:10.1161/01.hyp.7.3.386

Cited by 70 publications

(19 citation statements)

References 16 publications

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“…53 Our finding of lower cGMP production by the in vitro incubation of glomeruli from 16-week-old SHR, together with a decreased density of glomerular ANF binding sites, suggests that the down-regulated receptor population is that associated with guanylate cyclase. Our results are compatible with those of Marsh et al, 54 who noted lower basal and ANF-stimulated urinary cGMP secretion rates in conscious SHR.…”

Section: Discussionsupporting

confidence: 94%

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Glomerular atrial natriuretic factor receptors in spontaneously hypertensive rats.

et al. 1989

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There are differences in the renal handling of sodium between spontaneously hypertensive rats (SHR) and their normotensive controls. We investigated whether this difference may be associated with changes in plasma and tissue atrial natriuretic factor (ANF) levels and with alterations in glomerular ANF receptors at 4, 8, 12, and 16 weeks of age. Age-matched Wistar-Kyoto (WKY) and Wistar rats were used as normotensive controls. Systolic blood pressure was higher in SHR at 8, 12, and 16 weeks, and cardiac hypertrophy was also present in these animals at 4 weeks. Plasma ANF C-and N-terminal concentrations were greater than in both normotensive groups at 8 and 16 weeks. ANF in the right atrium was higher in SHR than in WKY rats and identical to that in the Wistar group at 4 and 8 weeks. ANF in the left atrium was lower in SHR than in both control groups at week 12. No differences were found in ventricular ANF content. The density of glomerular ANF binding sites increased with age in WKY and Wistar rats but not in SHR. At weeks 8, 12, and 16, both normotensive groups had a higher density of binding sites than SHR, but binding site affinity was greater in SHR at weeks 8 and 12. After incubation with increasing concentrations of ANF, the production of cyclic guanosine monophosphate (cGMP) by isolated glomeruli from 16-week-old rats was lower in SHR than in both normotensive groups. We conclude that the development of hypertension in SHR is associated with higher plasma ANF levels and decreased glomerular ANF receptor density and glomerular cGMP production. Through modulation of ANF glomerular receptors, ANF in SHR, when compared with normotensive counterparts, may contribute to the difference in renal sodium handling. (Hypertension 1989; 13:567-574)

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Section: Discussionsupporting

confidence: 94%

“…54 In higher doses, a marked drop in blood pressure is observed in SHR accompanied by lower diuresis and natriuresis than in normotensive controls. This decrease of natriuresis with higher doses of ANF could be explained by a reduction in renal perfusion pressure, a well-known factor mediating the effect of the peptide.…”

Section: Discussionmentioning

confidence: 98%

Glomerular atrial natriuretic factor receptors in spontaneously hypertensive rats.

et al. 1989

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“…In those studies, 15 the complete depressor dose-response relation for exogenous ANF and the dose-related potentiation of that activity by SQ 29,072 were characterized in conscious SHR, a model in which ANF produced a larger depressor response than in normotensive rats. 17 The present experiments extended that earlier work by examination of the renal responses to depressor doses of ANF-(99-126) in conscious, unrestrained SHR and provided additional evidence that a specific NEP inhibitor may prevent inactivation of ANF in vivo.…”

Section: Potentiation Of Renal Effects Of Atrial Natriuretic Factor-(supporting

confidence: 75%

Potentiation of renal effects of atrial natriuretic factor-(99-126) by SQ 29,072.

Seymour¹,

Fennell²,

Swerdel³

1989

Hypertension

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Depressor and renal activities of atrial natriuretic factor-(99-126) were determined in conscious, unrestrained spontaneously hypertensive rats treated with a neutral endopeptidase inhibitor, SQ 29,amino]heptanoic acid). SQ 29,072 (100 /tmol/kg i.v.) prolonged the transient depressor effects of the peptide for as long as 2 hours. During the first hour after 3, 10, and 30 nmol/kg atrial natriuretic factor, urinary excretion of cyclic 3'5' guanosine monophosphate was significantly increased by 9.2±3.4, 13.0±2.2, and 12.7±4.2 nmol/kg/hr, respectively, in vehicle-treated rats and by 26.9±7.9, 52.1±11.1, and 46.4±12.2 nmol/kg/hr, respectively, in rats given 100 /tmol/kg SQ 29,072. During the first hour after 3 and 10 nmol/kg atrial natriuretic factor-(99-126), the sodium loss was 161±56 and 139±42 /teq/kg/hr in vehicle-treated rats and was significantly greater (694±316 and l,038±135 /teq/kg/hr) in rats given 100 /tmol/kg SQ 29,072. After administration of 3, 10, and 30 /tmol/kg SQ 29,072, the area over the curves of the depressor responses to 3 nmol/kg of the peptide increased from 297±70 to 306±108, 440±143, and 669±186 mm Hgmin, respectively, while the concurrent natriuretic responses rose from 161±56 to 250±88,332±142, 464±164, and 694±316 /teq/kg/hr. In summary, the neutral endopeptidase inhibitor SQ 29,072 increased the magnitudes and especially the durations of the depressor, natriuretic, and cyclic guanosine monophosphate responses to exogenous atria] natriuretic factor-(99-126) in conscious spontaneously hypertensive rats, presumably by inhibition of degradation of atrial natriuretic factor in vivo. In conclusion, neutral endopeptidase inhibition offers an important new technique for enhancement and prolongation of the biological lifetime of atrial natriuretic factor. (Hypertension 1989;14:87-97)

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“…Injection or sustained infusion of ANF showed a greater 11 or no 3 difference in systemic blood pressure drop in SHR, but there have been no reports on the response of pulmonary arterial pressure to ANF in SHR. Jin et al 23 showed the pulmonary depressor effect of ANF was significantly greater in hypoxia than in SL control Sprague-Dawley rats; however, there was no significant difference between experimental and control rats in the reduction of systemic arterial pressure.…”

Section: Discussionmentioning

confidence: 97%

Effects of atrial natriuretic factor in chronic hypoxic spontaneously hypertensive rats.

et al. 1991

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The present study was designed first to investigate the pulmonary hypertensive effects of chronic hypoxia in spontaneously hypertensive rats and second to compare the cardiovascular effects of atrial natriuretic factor on rats exposed to hypoxia and on control rats kept at sea level. Catheters were placed in the femora] and pulmonary arteries for measurement of mean systemic arterial pressure and mean pulmonary arterial pressure. The cardiac output was measured by thermodilution method. It was found that 4 weeks of simulated 18,000-foot hypoxia led to polycythemia, right ventricular hypertrophy, and pulmonary hypertension, which resulted from an increased pulmonary vascular resistance. However, systemic arterial pressure was not significantly different between the two groups of rats. Atrial natriuretic factor administration decreased systemic arterial pressure and pulmonary arterial pressure to a lesser extent in the hypoxic group compared with the sea level control group. It is concluded that these animals snowed an impaired response to atrial natriuretic factor after long-term exposure to hypoxia. (Hypertension 1991;18u355-359) A trial natriuretic factor (ANF) possesses potent vasorelaxant properties in blood vessels and natriuretic and diuretic effects in the kidney after exogenous administration as well as endogenous release.1 Changes in plasma ANF concentration or the sensitivity to ANF have been shown to be associated with alterations of body fluid 2 "4 and with diseases such as nephrotic syndrome, 56 experimental cirrhosis, 7 bile duct ligation, 8 and especially hypertension. Tikkanen et al 9 showed that NaCl and deoxycorticosterone acetate-NaCI loading increased plasma ANF levels and that elevated blood pressure did not stimulate ANF release further. Sonnenberg et al 10 reported a decreased atrial content of ANF in the spontaneously hypertensive rat (SHR), but Pettersson et al 4 showed that basal plasma ANF levels were similar in the SHR and Wistar-Kyoto rats. Nevertheless, most reports agreed that the increase in plasma ANF was attenuated during acute volume expansion in SHR rats.2 -4 The sensitivity of blood pressure drop after exogenously administered ANF in the normotensive and hypertensive rats is also controversial.3 ' 1112 ANF may play an important role Received October 15, 1990, accepted in revised form April 29, 1991. in the pulmonary hypertension induced by hypoxia. 13Acute hypoxia stimulates the release of ANF from isolated hearts 14 and increases plasma ANF in anesthetized rabbits 15 and pigs. 16 In the chronic hypoxia of widespread lung disease or high altitude residents or animals pulmonary hypertension, ventricular hypertrophy, and polycythemia may develop. 17 In rats exposed to 21 days of hypoxia, the left atrial ANF content was significantly increased, whereas right atrial ANF content was significantly reduced, and plasma ANF concentration was elevated compared with air control animals. 18ANF has a direct effect on the pulmonary vasculature, causing relaxation of isolated segments of...

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Renal and blood pressure responses to synthetic atrial natriuretic factor in spontaneously hypertensive rats.

Cited by 70 publications

References 16 publications

Glomerular atrial natriuretic factor receptors in spontaneously hypertensive rats.

Glomerular atrial natriuretic factor receptors in spontaneously hypertensive rats.

Potentiation of renal effects of atrial natriuretic factor-(99-126) by SQ 29,072.

Effects of atrial natriuretic factor in chronic hypoxic spontaneously hypertensive rats.

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