Hypertension systemic

Glomerular damage Accelerated hypertension Systemic lupus erythematosus Poststreptococcal glomerulonephritis Antiglomerular basement membrane disease... 

Because side effects can complicate the use of corticosteroids, a careful history and certain tests may be advisable, particularly if a patient may require prolonged ocular therapy. Steroids should be used with great caution in patients with diabetes mellitus, infectious disease, chronic renal feilure, congestive heart feilure, and systemic hypertension. Systemic administration is generally contraindicated in patients with peptic ulcer, osteoporosis, or psychoses. Topical steroids should be used with caution and only when necessary in patients with glaucoma. 

Hartleb, M., Michielsen, RR, Dziurkowska-Marek, A. The role of nitric oxide in portal hypertensive systemic and portal vascular pathology. Acta Gastroenterol. Belg. 1997 60 222 - 232... 

Transdermal clonidine (clonidine TTS) has been used with some success for the treatment of mild hypertension. Systemic adverse effects are similar to those seen after oral administration, but are less frequent and milder. They include dry mouth, drowsiness, headache, sexual disturbance, cold extremities, obstipation, and fatigue (31-33). These adverse effects rarely necessitate withdrawal of clonidine TTS. 

Cortisol-Cortisone Conversion. Under normal conditions, this equilibrium slightly favors the oxidized compound. Similarly, the conversion of corticosterone to 11-deoxycorticosterone is also mediated by the liP-hydroxysteroid dehydrogenase enzyme system and requites NAD(P) /NAD(P)H. This conversion is especially important both in the protection of the human fetus from excessive glucocorticoid exposure, and in the protection of distal nephron mineral ocorticoid receptors from glucocorticoid exposure (14). The impairment of this conversion is thought to result in hypertension associated with renal insufficiency (15). 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

Cardiomyopathy. Cardiomyopathy, or diseased heart muscle, may reach a point at which the heart can no longer function. It arises from a combination of factors, including hypertension, arrhythmias, and valve disease. Other problems, such as congestive heart failure, cause the interrelated heart—lung system to break down. Because the heart can no longer adequately pump, duid builds up in the lungs and other areas. 

Despite the limitations imposed by the physiology of the skin, several marketed controUed release transdermal dmg dehvery systems are available in the United States for example, scopolamine [51-34-3] for the treatment of motion sickness, nitroglycerin [55-63-0] for angina, estradiol [50-28-2] for the rehef of postmenopausal symptoms and osteoporosis, clonidine [4205-90-7] for the treatment of hypertension, fentanyl [437-38-7] as an analgesic, and nicotine [54-11-5] as an aid to smoking cessation. These systems are designed to dehver dmg for periods of one to seven days. 

Histamine is the biological amine, playing an important role in living systems, but it can also cause unnatural or toxic effects when it is consumed in lai ge amounts. It can occur with some diseases and with the intake of histamine-contaminated food, such as spoiled fish or fish products, and can lead to undesirable effects as headache, nausea, hypo- or hypertension, cai diac palpitations, and anaphylactic shock syndrome. So, there is a need to determine histamine in biological fluids and food. 

Angiotensin converting enzyme (ACE) plays a central role in cardiovascular hemostasis. Its major function is the generation of angiotensin (ANG) II from ANGI and the degradation of bradykinin. Both peptides have profound impact on the cardiovascular system and beyond. ACE inhibitors are used to decrease blood pressure in hypertensive patients, to improve cardiac function, and to reduce work load of the heart in patients with cardiac failure. 

In some patients with hypertension and in all patients with cardiac failure, the renin-angiotensin system is activated to an undesired degree, burdening the heart. The consequences of diminished ANG II generation by ACE inhibitors are multiple. In patients with hypertension, blood pressure is reduced as a result... 

Bader M, Paul M, Fernandesz-Alfonso M et al (1994) Molecular biology and biochemistry of the renin-angiotensin system, Chap. 11. In Swales ID (ed) Textbook of hypertension. Blackwell Scientific Publications, Oxford, London, Edinburgh, pp 214-232... 

Bader M, Peters J, Baltatu O et al (2001)Tissue renin-angiotensin systems new insights from experimental animal models in hypertension research. J Mol Med 79 76-102... 

The substrate specificity of ACE is low. ACE cleaves a variety of pairs of amino acids from the carboxy-terminal part of several peptide substrates. The conversion of ANGI to ANGII and the degradation of bradykinin to inactive fragments are considered the most important functions of ACE. Both peptides have profound impact on the cardiovascular system and beyond. ACE is thus an important target for ACE inhibitors. These compounds are frequently and efficiently used in the treatment of hypertension and cardiac failure. 

Ca2+ is an important intracellular second messenger that controls cellular functions including muscle contraction in smooth and cardiac muscle. Ca2+ channel blockers inhibit depolarization-induced Ca2+ entry into muscle cells in the cardiovascular system causing a decrease in blood pressure, decreased cardiac contractility, and antiarrhythmic effects. Therefore, these drugs are used clinically to treat hypertension, myocardial ischemia, and cardiac arrhythmias. 

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. 

Kuznetsova T, Staessen JA, Thijs L et al (2004) European Project On Genes in Hypertension (EPOGH) Investigators. Left ventricular mass in relation to genetic variation in angiotensin II receptors, renin system genes, and sodium excretion. Circulation 110 2644-2650... 

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