Background and objectives: Diabetes mellitus is a long term disease with variable clinical manifestation and progression. The prevalence of diabetes mellitus in India was found to be 2.4 % in rural and 4 - 11.6 % in urban. It leads to number of complications like cardiovascular, renal, neurological, ocular and others such as intercurrent infections. Therefore understanding the pathophysiology of hypertension and diabetes is important.Hence this study is taken up to estimate Serum Nitrate levels in Type II Diabetic Patients with Hypertension compared with healthy individuals. Methodology: The present study was conducted in the Department of Physiology, Al-Ameen Medical College, Bijapur and District Hospital, Bijapur. Thirty five Type II Diabetic Patients with Hypertension (35) between 35 to 65 yrs age and Thirty nine (39) healthy individuals, controls between 38 yrs to 65 yrs age visiting Al-Ameen Medical College Hospital, Bijapur and District Hospital Bijapur were selected. Serum Nitrate was estimated by GRIESS METHOD. Statistical analysis was done by ANOVA and unpaired t test. Results: Statistically significant variations were found in parameters like age, Ht, Wt, BSA, BMI, PR, SBP, DBP, Serum Nitrate levels in controls and Primary Hypertension patients. Interpretation and conclusion: In the present study the mean ± SEM of Serum Nitrate in controls was found to be 49.93 ± 1.01 μ mol / lt, and Type II Diabetic patients with Hypertension was 29.36 ± 1.29 μ mol / lt. It was found Serum Nitrate levels of Type II Diabetic patients with Hypertension was lower when compared with the controls, these difference were found to be statistically significant (t =15.324, p= 0.0000). Mechanism which can reduce NO levels in Diabetic patients with Hypertension are decreased eNOS activity and thus reduces the bioavailability of NO and also increased oxidative stress. ADMA is an endogenous inhibitor of eNOS thus elevated ADMA will further decrease the bioavailability of NO. Elevated CRP has been reported to decrease the stability of mRNA for eNOS, thus further reducing the synthesis of NO.