Renal vasodilatation in response to acute volume load is attenuated following lesions of parvocellular neurones in the paraventricular nucleus in rats.

The effect on the cardiovascular response to volume load, of lesioning the paraventriculo-spinal projection to the lower thoracic cord, has been investigated in urethane-anaesthetised rats. In control animals volume loading with 4% Ficoll 70 in 165 mM NaCl at 0.6 ml/min i.v. up to 1% body weight produced a pressor response and tachycardia accompanied by a vasodilatation in the renal vascular bed. Injections of 2-4 micrograms ibotenic acid in 100-200 microliters solution were made into the paraventricular nucleus to lesion parvocellular neurones. When tested 3 days after the lesioning procedure, the renal vasodilator component of the response to volume load was abolished, although blood pressure and heart rate still rose. When the response to volume load was tested 28 days after the lesion, some degree of functional recovery appeared to have taken place. In these rats there was a weak renal vasodilation although the maximal increase in renal vascular conductance (20 +/- 13%) was still smaller than in the control animals. The efficacy of the lesioning procedure was verified by counting the number of fluorescent labelled neurones in PVN after injection of 1-2 microliters of a 1.25% solution of the retrograde marker 4,6 diamidino-2-phenyl indole (DAPI) bilaterally into the cord at T8-10. 1005 +/- 63 neurones were present in each side of PVN in non-PVN-lesioned rats whilst in lesioned animals only 444 +/- 153 cells were present. These results suggest that the paraventriculo-spinal projection to the lower thoracic cord may play an important role in sympathetically mediated changes in renal blood flow during the early phase of the response to an acute volume load.