trace the relationshp of d renin angiotensin-aldosterone mechnism 2 hypertension?
603253
Angiotensin II doesn't cause reabsorbtion of NaCl, it is a generalized vasoconstrictor and causes the release of Aldosterone, a mineralcorticoid, from the adrenal cortex.\n\nHigh levels of body Potassium, in addition to decreased renal blood flow or blood pressure cause the release of Renin from the Juxtaglomerular Apparatus. Renin converts circulating Angiotensinogen to Angiotensin I, which is converted, via Converting Enzyme in the lungs, to Angitensin II, which causes vasoconstriction and the release of Aldosterone. Aldosterone causes the reabsorbtion of Sodium Ions and the Excretion of Potassium at the Distal Convoluted Tubule and Collecting Tubule. This happens via activated Na/K ATPases or active transport of Na into the tissue spaces from the lumen of the nephron. Na is the most osmotically active solute, so water follows. Na and water are picked up by the Vasa Recta and peritubular capillaries, and blood volume increases. This mechanism is normally used to raise blood pressure that has fallen, but if there is an over-secretion of mineralocoricoids, as in Cushings syndrome (which is actually an over secretion of ACTH by a petuitary tumor, not aldosterone), hypertension can result.
1093577
there is no direct relationship with the two, however is does not mean that both cannot be elevated, high blood pressure is caused by many different things , and something the cause high blood pressure may sometimes also be equated to having cause a higher hemo count. but  the two are not directly proportionate
1038065
Plz read n learn\n\nhttp://www.google.co.uk/search?hl=en&q=What+are+the+different+effects+of+high+blood+pressure+and+other+cardiovascular+diseases&btnG=Search&meta=
426220
Class: ACE Inhibitor, Antihypertensive \n\nFDA labeled indications: Congestive heart failure, Hypertension, Impaired left ventricular function, Asymptomatic \n\nSide effects: Cardiovascular: Hypotension \nDermatologic: Rash \nEndocrine metabolic: Hyperkalemia \nGastrointestinal: Nausea and vomiting \nNeurologic: Asthenia, Dizziness \nRespiratory: Cough \n\nLess effective in black population than non-blacks
810354
Hypertension can multi-system effects. It is a risk factor for stroke and heart disease. Hypertension can increase the workload that the heart has to pump against, the heart overtime can develop what health care professionals call left ventricular hypertrophy (the left ventricle of the heart becomes overly thickened) which can lead to heart failure. Patients with heart failure will present with shortness of breath, fatigue, swelling of the legs, chest  pain etc due to the heart's inability to pump adequate amounts of oxygenated blood to meet the the body's physiological needs. \n\nHypertension is a modifiable risk factor for heart disease and stroke which can be controlled with lifestyle modification such as diet and exercise, medications and proper care of a trained healthcare professional.  Hope this helps.
453898
There is a lot to find about adderall and its side effects if you google for it on the net. \nAlthough you can find a lot of info, i would advise you to consult your doctor who prescribed you the meds to see if the 'mixing' of the medicines you are taking can be the cause of the seemingly controlled blood pressure.\nFYI I've added a link to a very good page about adderall, the effects, side effects etc, but again, best advice i can give you, is consult your doctor.\nGood luck,\nTiff
401254
Aldosterone is secreted in response to low extracellular sodium and acts on the distal tubule to increase the reabsorption of sodium from the urinary filtrate. I'm not sure where on the distal tubule though, if that's what you're asking...
87187
essential hypertension!
377549
Hypertension means high blood pressure. This generally means:\n\nSystolic blood pressure is consistently over 140 (systolic is the "top" number of your blood pressure measurement, which represents the pressure generated when the heart beats)\nDiastolic blood pressure is consistently over 90 (diastolic is the "bottom" number of your blood pressure measurement, which represents the pressure in the vessels when the heart is at rest)\nEither or both of these numbers may be too high.\n\nBlood pressure is determined by the amount of blood pumped by the heart, and the size and condition of the arteries. Many other factors can affect blood pressure, including volume of water in the body; salt content of the body; condition of the kidneys, nervous system, or blood vessels; and levels of various hormones in the body.\n\nEssential hypertension has no identifiable cause. It may be caused by genetics, environmental factors, or even diet, such as how much salt you use.\n\n"Secondary" hypertension is high blood pressure caused by another disorder. This may include:\n\nadrenal gland tumors\nCushing's syndrome\nkidney disorders\nglomerulonephritis (inflammation of kidneys)\nrenal vascular obstruction or narrowing\nrenal failure\nuse of medications, drugs, or other chemicals\noral contraceptives\nhemolytic-uremic syndrome\nHenoch-Schonlein purpura\nperiarteritis nodosa\nradiation enteritis\nretroperitoneal fibrosis\nWilms' tumor
902832
our kidneys also control the blood pressure in our bodies by secreting a hormone called renin.
641837
Hormone Control of Water and Salt \nWater reabsorption is controlled by the antidiuretic hormone (ADH) in negative feedback. ADH is released from the pituitary gland in the brain. Dropping levels of fluid in the blood signal the hypothalamus to cause the pituitary to release ADH into the blood. ADH acts to increase water absorption in the kidneys. This puts more water back in the blood, increasing the concentration of the urine. When too much fluid is present in the blood, sensors in the heart signal the hypothalamus to cause a reduction of the amounts of ADH in the blood. This increases the amount of water absorbed by the kidneys, producing large quantities of a more dilute urine.\n\nAldosterone, a hormone secreted by the kidneys, regulates the transfer of sodium from the nephron to the blood. When sodium levels in the blood fall, aldosterone is released into the blood, causing more sodium to pass from the nephron to the blood. This causes water to flow into the blood by osmosis. Renin is released into the blood to control aldosterone.
1048037
Drink 15 glasses of water a day, eat bananas & other fruits for the Potassium 2 a day. Fish oil, Sardines Salmon Omega-3's, Magnesium Gluconate- Relaxes arteries,Coenzyme Q 10-nutrient, Walk 30 minutes aerobic 4 times a week,Hawthorn 250 milligrams extract daily and finally Garlic 2 or 3 cloves a day minimum
129121
You're on the right track, but you haven't got it right yet.  Calcium is neccessary in muscle fibers (cells) to contract.  I believe calcium channel blockers block the entry into smooth muscle cells, in the walls of arterioles, from the plasma.  This decreases contraction by these fibers, and thus decreases vasoconstriction.  The result is vasodilatation.  This expansion of the lumens (the hole inside the small artery on cross section) of arterioles all over the body, decreases peripheral vascular resistance, and this lowers the blood pressure.  Whew!  These drugs may also decrease the contractility or strength of contraction of the heart, which would tend to lower blood pressure as well.  Now as far as the precise subcellular mechanism, I'm a little rusty.  I'm sure it's available if you google it in.  I'm just giving you what I know as a practicing ER doc.  My favorite class of drugs for lowering blood pressure are the ARBs (angiotensin receptor blockers).  I don't believe that the calcium channel blockers ever lower the serum calcium.  I've never noticed that.  I know that if a patient is overdosed on calcium channel blockers, you can reverse it somewhat by giving IV calcium.  In addition to their use for lowering blood pressure, some calcium channel blockers are used to slow the ventricular rate in supraventricular tachycardias, such as paroxysmal supraventricular tachycardia, atrial flutter, and atrial fibrillation.  We always have some concern with these drugs, if the patient has some heart failure, ie. a weak heart muscle, in that they may decrease the contractility of the heart and throw them into overt heart failure.  We don't have that concern with the ACE inhibitors and the ARB's.  The ACE inhibitors have a frequent side effect of causing a nagging cough, because they cause a buildup of histamine, but the ARB's don't have that problem.
921371
PLAB  \n... · gpvts · mrcgp · mrcog · mrcp · mrcpath · mrcpch · mrcs · plab · toefl · usmle ... DM - Gastroenterology DM - Neurology DM Endocrinology DM Nephrology DNB Part 1 ...www.rxpgonline.com/plab.html \nDNB Forums  \n... · gpvts · mrcgp · mrcog · mrcp · mrcpath · mrcpch · mrcs · plab · toefl · usmle ... DM - Gastroenterology DM - Neurology DM Endocrinology DM Nephrology DNB Part 1 ...www.rxpgonline.com/forum29.html
751385
It's called caduet.  It's a combination of:\n\nAmlopidine:  calcium channel blocker for hypertension.\n-look out for dizzyness, heart palpitation-generally, a very well tolerated blood pressure med\n\nAtorvastatin: To lower high cholesterol.\n-report immediately any muscle soreness, or cramping\n\n\nhttp://www.caduet.com/
856515
My mom needs to lower her blood pressure, and she is limiting salt as well as eating more fiber. . .oatmeal, cheerios.  Drink a lot of water, too, that is soooo important.
185017
Altered hemodynamic response to isosorbide dinitrate in essential hypertension\nBM Pannier, T Kando, AA Safarian, RN Isnard, BE Diebold, and ME Safar\n\nRelaxation produced by nitrates on venous, arteriolar, and large arterial vessels is well known but has never been studied in human hypertensive aortas studied in vivo. In this investigation, the effects of acute oral administration of 20 mg of isosorbide dinitrate were evaluated in 12 patients with sustained essential hypertension and nine normotensives of the same age. Noninvasive measurements of systolic, diastolic, and mean arterial pressure, carotid-femoral pulse wave velocity and aortic-arch diastolic diameter using suprasternal echocardiography were determined before and 3 hours after drug administration. In normal subjects, isosorbid dinitrate significantly decreased systolic blood pressure and pulse pressure but did not affect diastolic and mean arterial pressure. In contrast, in hypertensives, the same dosage of isosorbid dinitrate decreased together systolic, diastolic mean, and pulse pressure. In both populations, pulse wave velocity decreased significantly whereas aortic arch diastolic diameter increased markedly. The increase was observed mainly in normal subjects. The study provided evidence that (1) both in normal subjects and hypertensives, isosorbide dinitrate caused an increase in aortic diameter together with an increase in arterial distensibility; and (2) the changes in mean arterial pressure were significant only in hypertensives, indicating that the altered vasodilator response in essential hypertension is not endothelium-mediated