On the role of atrial natriuretic peptide in cardiovascular regulation in the spontaneously hypertensive rat.
Atrial natriuretic peptide ANP(1-23) reduced mean arterial pressure (MAP), cardiac output (CO), central blood volume (CBV) and stroke volume (SV) when given i.v. (100 pmol/min) to spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). In SHR, total peripheral resistance (TPR) was significantly lowered. The major cause of the fall in blood pressure in WKY was reduction in CO and in SHR reduction in TPR. Acute 20% volume expansion increased plasma immunoreactive ANP (IR-ANP) in WKY as well as in SHR. However, the ANP release in SHR was blunted compared with WKY. After chronic high salt intake, ANP release in SHR was even further reduced in relation to an acute volume load. We conclude that the release of ANP as well as the haemodynamic responses to exogenous ANP is altered in SHR.
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000502:physiology*; D001794:Blood Pressure; D005440:Fluid Therapy; D006439:Hemodynamics; D006973:Hypertension / Q000235:genetics* / Q000503:physiopathology; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D011919:Rats, Inbred Strains / Q000502:physiology*; D011921:Rats, Inbred WKY; D012965:Sodium Chloride / Q000008:administration & dosage
D012965:Sodium Chloride; D009320:Atrial Natriuretic Factor