Are renovascular effects of sympathetic cotransmitters ATP and NPY age-dependent in spontaneously hypertensive rats?
Neuronally released NPY plays a major role in potentiating RNS-induced nonadrenergic pressor responses in kidneys of WKY and young SH-SP rats. In adult SH-SP rats NPY fails to enhance these responses. In this hypertensive model ageing seems to be associated with a loss of a modulatory role of renal NPY Y1 receptors. Since pressor responses to NE and ATP are higher in SH-SP animals, functional NPY-Y1 receptor downregulation might be an adaptive mechanism.
Long-term alcohol consumption did not cause chronic pancreatitis but impaired exocrine pancreatic function. The mechanism behind it could be associated with decreased output of intestinal CCK and lower concentration of pancreatic CCK. Furthermore, the nonoxidative pathway of ethanol metabolism was probably involved in it.