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Biotech / Medical : Biotech Valuation -- Ignore unavailable to you. Want to Upgrade?

To: Biomaven who wrote (22572)	1/18/2007 2:47:13 PM
From: former_pgs	Read Replies (1) \| Respond to of 52153

OT: For those interested in the question of hypertension, the following is a great paper. Very nicely designed experiments for a very important question. May have some impact for those in speedel as well. Distinct roles for the kidney and systemic tissues in blood pressure regulation by the renin-angiotensin system. Crowley SD, Gurley SB, Oliverio MI, Pazmino AK, Griffiths R, Flannery PJ, Spurney RF, Kim HS, Smithies O, Le TH, Coffman TM. Division of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, North Carolina 27705, USA. Angiotensin II, acting through type 1 angiotensin (AT(1)) receptors, has potent effects that alter renal excretory mechanisms. Control of sodium excretion by the kidney has been suggested to be the critical mechanism for blood pressure regulation by the renin-angiotensin system (RAS). However, since AT(1) receptors are ubiquitously expressed, precisely dissecting their physiological actions in individual tissue compartments including the kidney with conventional pharmacological or gene targeting experiments has been difficult. Here, we used a cross-transplantation strategy and AT(1A) receptor-deficient mice to demonstrate distinct and virtually equivalent contributions of AT(1) receptor actions in the kidney and in extrarenal tissues to determining the level of blood pressure. We demonstrate that regulation of blood pressure by extrarenal AT(1A) receptors cannot be explained by altered aldosterone generation, which suggests that AT(1) receptor actions in systemic tissues such as the vascular and/or the central nervous systems make nonredundant contributions to blood pressure regulation. We also show that interruption of the AT(1) receptor-mediated short-loop feedback in the kidney is not sufficient to explain the marked stimulation of renin production induced by global AT(1) receptor deficiency or by receptor blockade. Instead, the renin response seems to be primarily determined by renal baroreceptor mechanisms triggered by reduced blood pressure. Thus, the regulation of blood pressure by the RAS is mediated by AT(1) receptors both within and outside the kidney. ncbi.nlm.nih.gov

To: Biomaven who wrote (22572)	1/18/2007 3:00:12 PM
From: Ian@SI	Read Replies (1) \| Respond to of 52153

Sounds like blood sugar. In different people, exercise can cause blood sugar readings to go up, down, or remain unchanged. I only discovered this after about a dozen blood tests (A1C normal, Fasting - high). I was incorporating my workout with the trip to the doctor. After running to his office, he'd send me next door for the blood test which would be high if taken within an hour of getting there. This business would be a whole lot easier if we just had one standard!!! <G>

To: Biomaven who wrote (22572)	1/18/2007 9:31:20 PM
From: tom pope	Read Replies (1) \| Respond to of 52153

Salt bp link- Anecdotal - not for me. For years I've been resisting my doctor's urgings to cut down on salt (how could I, I would retort, it's not possible to walk down a grocery store aisle without picking up a ton of salt), but about a month ago I decided to give in to him and abjure the use of table salt with meals. It's made a ten point average bp difference. Wrong answer, dammit, I love to salt my meals! I wonder whether anybody has ever examined whether salt is habit-forming?