Glucose is a key fuel and an important metabolic substrate in ammals. A number of mechanisms contribute to the changes in cellular functions that occur in response to exposure of endogenous factors. These include increased cytokines and growth factors as well as the glucose specific effects due to increased intracellular level of glucose. The kidneys play a major role in the regulation of plasma glucose levels, and ever increasing attention is now being given to renal glucose transporters as the implications including diabetes mellitus. The primary rabbit renal proximal tubule cells (PTCs) culture system utilized in my study has well recognized to retain in vitro the differentiated phenotype typical of the renal proximal tubule, including a polarized morphology and distinctive proximal tubule transport. Thus, I examined the effects of several actors on Na＋/glucose cotransporters in PTCs. ANG II, EGF, epinephrine, TCDD, high glucose, bee venom, partially inhibited [14C]-α-methyl-D-glucopyranoside (α-MG) uptake, whereas BSA stimulates α-MG uptake in PTCs. On the other hand, caffeic acid, ginsenosides, and estrogens protected oxidative stress-induced inhibition of α-MG uptake.

• Kidney
• Na(+)/glucose cotransporter
• Glucose

Hypertension is a polygenic and multifactorial disease and is intimately related to salt homeostasis. Four important vasoactive peptide systems participate in regulating blood pressure and salt homeostasis. Their interplay is indispensible in many physiologic and pathologic conditions. While the renin-angiotensin and the endothelin systems raise blood pressure by inducing vasoconstriction and sodium retention (or excretion), the kallikrein-kinin and the natriuretic peptide systems reduce blood pressure by eliciting vasodilatation and natriuresis. Gene targeting as well as transgenesis have provided us a lot of information on the biological functions of the genes of these systems. Animal models from these technologies are discussed in relation to blood pressure regulation.

• Transgenesis
• Knockout
• Hypertension
• Angiotensin
• Endothelin
• Kinin
• Natriretic peptide
• Homeostasis

Adrenomedullin (AM) is a multi-functional peptide discovered in human pheochromocytoma. Initially, it was suggested that AM was synthesized only by tumor cells, however, subsequent studies revealed that it was produced also by normal adrenal medulla as well as by many other tissues. Now it is well established that AM functions as a circulating hormone and local paracrine mediator with multiple biological activities. AM stimulated cAMP production in human platelets and exerted potent and long-lasting hypotensive activity in the rat. AM is a physiologically relevant regulator in fluid and electrolyte homeostasis; inhibition both water and salt intake, increase renal blood flow, and cause diuresis and natriuresis. The up-regulation of cardiac AM system in hypertension may be a protective mechanism decreasing myocardial overload due to vasodilatory and natriuretic properties of AM, as well as limiting further myocardial hypertrophy and remodeling. AM may protect the kidney against ischemia-reperfusion injury. AM is also suggested as antiapoptotic, anti-inflammatory and angiogenic factor. In this review, I offer a review of our current knowledge on AM and give the putative role of AM in water-electrolyte balance, hypertension and kidney disease.

• Adrenomedullin
• Water-electrolyte balance
• Hypertension
• Kidney

Renal sodium handling is known as an important function that maintains both body fluid volume and blood pressure regulation. Recently, advances in molecular biology have led that alterations of tubular sodium handling are closely related to changes of blood pressure. Also, tubular sodium uptakes are controlled by any protein participating in its reabsorption and regulation, which are influenced by genetic, nutritional, metabolic and neurohormonal factors. All of these factors, alone or combination, may be able to impair the normal renal tubular sodium handling and develop high blood pressure. The investigations about the role of kidney in hypertension are shifting toward inherited as well as acquired tubular defects and further studies about renal sodium handling based on sodium transporters on the tubular segments will be needed. This review will discuss the relationship between renal sodium handling and hypertension.

• Kidney
• Sodium
• Hypertension

Evidence for a relationship between high sodium intake and high blood pressure comes from animal experimental studies, controlled clinical trials, and epidemiologic studies. Aanalyses from the International Co-Operative Study of Salt and Blood Pressure found estimates of systolic and diastolic blood pressure lower by 3 to 6 mmHg and 0 to 3 mmHg, respectively, for each lower daily sodium intake; the Dietary Approaches to Stop Hypertension-Sodium feeding trial showed that lower versus higher sodium reduced systolic blood pressure and diastolic blood pressure by 6.7 and 3.5 mmHg, respectively. Lowered sodium intake may help lower blood pressure and reduce or obviate the need for antihypertensive drugs. Most of studies suggest that potassium intake has inverse relationship on systolic and diastolic blood pressure; dietary potassium deficiency induces a salt sensitivity in the high incidence and prevalence of hypertension in African-Americans. Increased potassium intake reduces systolic and diastolic blood pressure; this effect is more enhanced in hypertensives compared to normotensives, and in those consuming a high intake of sodium. Increased potassium intake in combination with sodium restriction may provide the optimal means for prevention and treatment of hypertension. Increased potassium intake may reduce the risk of stroke independent of its effects on blood pressure.

• Sodium
• Potassium
• Hypertension
• Diet

Renal disease is closely associated with hypertension. Hypertension belongs to the clinical picture of chronic kidney disease (CKD). Hypertension associated with renal diseases occurs as a complication of various glomerular and interstitial diseases and may accelerate the decline of renal function if inadequately controlled. The pathophysiology through which the kidney raises blood pressure have been considerably clarified in recent years and it could be shown that “hypertension goes with the kidney” in experimental and clinical studies. The combined interactions of multiple independent mechanisms are thought to be involved in the development of hypertension. Impaired renal sodium handling leads to volume expansion. There is inappropriate activation of the renin-angiotensin system. As only recently documented in detail, renal injury raises the sympathetic tone, even when whole kidney glomerular filtration rate (GFR) is unchanged. This results from stimulating afferent signals coming from the kidney. There also is an evidence of impaired endothelial cell dependent vasodilatation even in very early stages of renal dysfunction. And other factors including uric acid, parathyoid hormone (PTH), and calcium may play a role in concert with other factors in the development of hypertension of renal diseases. Understanding these pathophysiologies is important for appropriate antihypertensive treatment.

• Hypertension
• Renal disease
• Renin-angiotensin system
• Sympathetic nerve system
• Chronic renal failure