No abstract

“The stability of the internal environment is the condition that life should be free and independent… So, far from the higher animal being indifferent to the external world, it is on the contrary in a precise and informed relation with it, in such a way that its equilibrium results from a continuous and delicate compensation, established as by the most sensitive of balances.” Claude Bernard (1865)

No abstract

Human postmortem studies as well as experimental animal studies indicate profound changes in the suprachiasmatic nucleus (SCN) in several pathological conditions. In addition, observations in experimental animals show that the SCN peptides, vasopressin (VP) and vasoactive intestinal peptide (VIP) are essential for adequate rhythmicity. These data prompted us to investigate whether changes in these neuronal populations are the cause or consequence of hypertension. Changes in blood pressure and levels of neuropeptide expression in the SCN were determined during the development of hypertension in spontaneous hypertensive rats (SHR), 2K1C reno-vascular induced hypertensive animals and their respective controls. During the pre-hypertensive stage (5 weeks of age), the VIP and AVP content was higher and the somatostatin (SOM) content was lower in the SHR SCN. At the onset of hypertension (12 weeks of age), when blood pressure levels had just reached ~140 mmHg, AVP and SOM content in the SCN was not different anymore in SHRs compared to control, but VIP was still higher. After 16 weeks, the AVP content was decreased, but SOM was increased and the overall level of VIP in the SCN was still higher in SHRs compared to controls. None of the aforementioned changes in the SCN was observed after induction of hypertension in the 2K1C model. However, while VIP was increased in the NTS projecting medial region of the SCN in SHR animals only after the establishment of hypertension, VIP was decreased in the same region in the 2K1C induced hypertensive rats. Consequently, the present findings confirm previous studies in human and rat indicating that changes in the SCN are strongly associated with the development of hypertension. In addition the changes in peptide content in the 2K1C animals indicate that the SCN is also able to respond to increases in blood pressure.