title: Effects of deoxycorticosterone on renal vascular reactivity and flow-pressure curve in spontaneously hypertensive rats.
abstract: The role of mineralocorticoids as sodium retaining hormones has been recently enlarged to include their function as modulators of cardiovascular function and injury. This study evaluated the contribution of possible functional changes in resistance vessels to the additional BP increase produced by the chronic administration of DOCA to SHR. The flow-pressure curve and renal responses to vasoconstrictors (phenylephrine [Phe] and angiotensin II [AII]) and vasodilators (acetylcholine [ACh] and nitroprusside [NP]) were characterized in isolated kidneys from Wistar Kyoto (WKY) and SHR treated or untreated with DOCA for nine weeks. DOCA increased BP in SHR but did not modify BP in WKY rats. Kidneys from SHR showed enhanced reactivity to Phe and AII that was not increased by DOCA. DOCA reduced sensitivity to AII in SHR. Responsiveness to ACh was increased in SHR and was not attenuated by DOCA in WKY or SHR. Vasodilator response to NP was not significantly affected by DOCA in WKY or SHR. The flow-pressure curve was markedly up-shifted in SHR when compared with kidneys from WKY rats. DOCA administration did not modify the flow-pressure curve in WKY but produced attenuation at low flow levels in SHR. Our results demonstrate that DOCA increases BP in SHR but does not increase the flow-pressure curve or renal vascular reactivity to vasoconstrictors, and does not reduce responsiveness to endothelium-dependent and independent vasodilators in SHR or WKY rats. Therefore, our data suggest that the BP increase produced by DOCA in SHR is not related to abnormalities in vascular function in resistance vessels.
authors.affiliation: Departamento de Fisiología, Facultad de Medicina, Servicio de Nefrología, Unidad Experimental, Hospital Virgen de las Nieves, Granada, Spain.
authors.forename: V
authors.initials: V
authors.lastname: Chamorro
authors.forename: J M
authors.initials: JM
authors.lastname: Moreno
authors.forename: R
authors.initials: R
authors.lastname: Wangensteen
authors.forename: J
authors.initials: J
authors.lastname: Sainz
authors.forename: I
authors.initials: I
authors.lastname: Rodriguez-Gomez
authors.forename: A
authors.initials: A
authors.lastname: Osuna
authors.forename: F
authors.initials: F
authors.lastname: Vargas
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage / Q000493:pharmacokinetics; D000804:Angiotensin II / Q000008:administration & dosage / Q000493:pharmacokinetics; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D003900:Desoxycorticosterone / Q000008:administration & dosage / Q000009:adverse effects / Q000493:pharmacokinetics*; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D007668:Kidney / Q000098:blood supply / Q000187:drug effects / Q000601:surgery; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009599:Nitroprusside / Q000008:administration & dosage / Q000493:pharmacokinetics; D010477:Perfusion / Q000379:methods; D010656:Phenylephrine / Q000008:administration & dosage / Q000493:pharmacokinetics; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology; D012082:Renal Veins / Q000187:drug effects* / Q000473:pathology / Q000502:physiology*; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
chemical_list: D000804:Angiotensin II; D009599:Nitroprusside; D010656:Phenylephrine; D003900:Desoxycorticosterone; D000109:Acetylcholine