High K diets will reduce stroke deaths in both hypertensive SHRsp rats and Dahl S rats by about 90%. This huge protection does not depend on a lowering of blood pressure. High K diets allow cerebral arteries to carry a high pressure without sustaining the expected wall lesions. High K diets also greatly reduce the incidence of cerebral hemorrhage and infarctions in SHRsp rats. The new questions are as follows: 1) In hypertensive, hypercholesterolemic rabbits, will a high K diet reduce the deposition of cholesterol esters into the walls of the aorta and the carotid, vertebral, and coronary arteries? Will the high K diet in these rabbits greatly reduce the albumin hyperpermeability defect in the endothelial layer of the carotid artery? In these rabbits will the high K diet reduce complement deposition in the walls of damaged arteries? 2) In the natural diet of prehistoric man there was a high content of K and Mg, possibly 4 times more than in modern human diets. It is clear that high K diets provide very strong protection against stroke deaths in hypertensive SHRsp and Dahl S rats. In these hypertensive rats will a high Mg diet alone also provide some protection against stroke deaths? And will the combination of semi-high or high K and high Mg (as in a hunter-gatherer diet) provide even more protection against stroke deaths than the semi-high or high K diet alone? 3) It is now clear that high K diets greatly protect against stroke deaths in both hypertensive SHRsp and Dahl S rats, providing the high K diet is started at 5 weeks of age, before cerebral lesions have developed. We will study whether the high K diet can still protect against stroke deaths in hypertensive SHRsp and Dahl S rats, even though the high K diet is not begun until the cerebral arteries have already sustained some lesions. 4) There has always been the enigma of advancing BP with increasing age in acculturated societies. We hypothesize that a typical """"""""civilized diet"""""""" has enough NaCl (2%) to gradually damage glomerular ultrafiltering membranes in susceptible individuals as they advance in years. This 2% NaCl diet will be studied during 10 months of feeding in Dahl S and R rats, and compared to a .15% NaCl diet. The effect of high K diets on this process will be studied. Items to be studied: a) GFR of isolated kidneys perfused at normotensive (125mmHg) inflow pressures, b) BP, c) analysis of arachidonic and adrenic acid in renal papilla triglycerides, a unique indicator of interstitial cell granules. Low secretion of the cells may encourage the rise in BP., d) albuminuria as an index of glomerular lesions, e) Na excretory response to atrial natriuretic peptide.
