Background: Diabetic nephropathy (DN) is one of the commonest etiologies for ESRD. Various studies suggest that diabetic nephropathy occurs due to the accumulation of advanced glycosylated end products (AGEs), the activation of isoforms of protein C kinase, etc. Correlation of renal arterial fl ow resistance, GFR, and progression towards ESRD in DN is not well narrated in literature. Therefore, the main object of the study was to assess renal arterial fl ow resistance in patients with DN and to compare it with patients having non-evident diabetic nephropathy. Methods: This is a case control study done in a retrospective manner in the central part of Rajasthan, India, based upon data collection of admitted patients. Arbitrarily, a record of 40 cases (all males) consisting of poorly controlled diabetic cases (Hba1C >10 %) without nephropathy (n=20, group A) was compared with records of diabetic cases with nephropathy (n=20, group B). Group B had been further subdivided according to CKD (chronic kidney disease) staging. Data were examined for vital parameters, Serum creatinine, e-GFR, R.I. (resistive index) in renal arterial Doppler, urine albumin. Results: Group A and group B were characteristically the same. In group B 7 cases had CKD 1(B1), 2 cases had CKD 2 (B2), 4 cases had CKD 3 (B3) and 7 cases had CKD 5(B5) stage. In group B there was a progressive rise in R.I. index parallel to decline in GFR, rise in albuminuria from B1 to B5 stage (p<0.001). These parameters were normal in group A. Conclusion: It is concluded that DN begins from an increase in resistance to fl ow in renal arteries primarily resulting from resistance in afferent arterioles due to the reduction in size. This reduction may be because of increased ACE/ basal sympathetic activity at the beginning. Later on, there is a further increase in resistance due to progressive deposition of AGE end products in afferent arterioles further reducing the size and hydrostatic pressure at the afferent arteriolar end, resulting in a progressive decrease in GFR. Simultaneously hypo-perfusion of kidney tissue activates the renin-angiotensin system further reduces fl ow and progresses the DN.

The global burden of hypertension and associated co-morbidities (cardiac failure, renal failure), is constantly rising despite the availability of newer drugs. Therefore, this study was planned to review the role of VMC (Vasomotor Center) in hypertension along with adding stress-relieving methods in lifestyle measures to prevent an epidemic of hypertension. For this purpose textbook of physiology, and various reference studies were used. The text-book of physiology suggests the location of VMC (Lower pons and medulla) and its functioning related to blood pressure regulation. It receives a signal from baroreceptors and produces either a decrease or an increase in blood pressure. The VMC is influenced by the cerebral cortex and hypothalamus. The pathophysiology suggests that possibly chronic stress, mental overwork disturbs the cortical influences to hypothalamus and shifts VMC to a higher level and that results in high basal sympathetic discharge and increased LV ejection force along with shifting of baroreceptors and renal mechanism to a new higher level which brings the blood pressure or whole body vasculature to the same high level resulting in hypertension. The repetition of the same process shifts BP even higher. The centrally acting drugs, mental rest, sound sleep and stress relieving methods like yoga, Vipassana, etc. may help to reduce cortical impulses and to bring VMC back to normal. VMC will automatically correct various BP control mechanisms and bring back BP to normal. Thus continuous efforts are needed to remove precipitating factors of hypertension. The methods to relieve stress and exhaustion must be employed in lifestyle for hypertension besides JNC guidelines.