Correlation between blood pressure and ACR in subjects with and without obesity and abdominal obesity.

<p>*p value was obtained by age-adjusted multiple regression analysis.</p><p>ACR, albumin–creatinine ratio; WC, waist circumference; HTN, hypertension; SBP, systolic blood pressure; DBP, diastolic blood pressure.</p><p>Correlation between blood pressure and ACR in subjects with and without obesity and abdominal obesity.</p

Adjusted odds ratios of HTN prevalence and control according to states of obesity.

<p>Odds ratios and 95% confidence intervals were obtained by multiple logistic regression analysis.</p><p>Model 1 was adjusted for age, sex, and body mass index.</p><p>*Model 2 was adjusted for the covariates of model 1 plus alcohol intake, smoking, exercise, income, education, and diabetes mellitus status in the analysis of HTN prevalence. From the analysis of HTN control, HTN medication was added to the covariates of model 2.</p><p>HTN, hypertension; ACR, albumin–creatinine ratio; WC, waist circumference.</p><p>Adjusted odds ratios of HTN prevalence and control according to states of obesity.</p

HTN control in subjects with and without obesity and abdominal obesity by tertile of ACR.

<p>P value for trend was <0.001 for the non-obese/high WC group only. P values were <0.05 between two groups; ACR <30 vs. 30≤ ACR <300, and ACR <30 vs. ACR ≥300 for the non-obese/normal WC group only. The p values and p values for trends were not statistically significant in the other three groups. HTN, hypertension; ACR, albumin–creatinine ratio; WC, waist circumference.</p

General characteristics of subjects with and without obesity and HTN.

<p>Data are presented as mean ± standard error (SE) or percentages (SE).</p><p>*p values were obtained by the chi-Square test and t-test.</p><p>**Log transformation and data are presented as geometric mean ± standard error (SE).</p>†<p>Controlled HTN means subjects who have BP <140/90 mmHg.</p><p>HTN, hypertension; BMI, body mass index; WC, waist circumference; SBP, systolic blood pressure; DBP, diastolic blood pressure; FBG, fasting blood glucose; TG, triglyceride; HDL-C, high density lipoprotein cholesterol; LDL-C, low density lipoprotein cholesterol; TC, total cholesterol; WBC, white blood cell; eGFR, estimated glomerular filtration rate; ACR, albumin creatinine ratio; DM, diabetes mellitus.</p><p>General characteristics of subjects with and without obesity and HTN.</p

Prevalence of HTN in subjects with and without obesity and abdominal obesity by tertile of ACR.

<p>All p values for trends were <0.001. All p values were <0.001 between two groups; ACR <30 vs. 30≤ ACR <300, and ACR <30 vs. ACR ≥300 at all groups. HTN, hypertension; ACR, albumin–creatinine ratio; WC, waist circumference.</p

Distinct neurochemical influences on fMRI response polarity in the striatum

The striatum, known as the input nucleus of the basal ganglia, is extensively studied for its diverse behavioral roles. However, the relationship between its neuronal and vascular activity, vital for interpreting functional magnetic resonance imaging (fMRI) signals, has not received comprehensive examination within the striatum. Here, we demonstrate that optogenetic stimulation of dorsal striatal neurons or their afferents from various cortical and subcortical regions induces negative striatal fMRI responses in rats, manifesting as vasoconstriction. These responses occur even with heightened striatal neuronal activity, confirmed by electrophysiology and fiber photometry. In parallel, midbrain dopaminergic neuron optogenetic modulation, coupled with electrochemical measurements, establishes a link between striatal vasodilation and dopamine release. Intriguingly, in vivo intra-striatal pharmacological manipulations during optogenetic stimulation highlight a critical role of opioidergic signaling in generating striatal vasoconstriction. This observation is substantiated by detecting striatal vasoconstriction in brain slices after synthetic opioid application. In humans, manipulations aimed at increasing striatal neuronal activity likewise elicit negative striatal fMRI responses. Our results emphasize the necessity of considering vasoactive neurotransmission alongside neuronal activity when interpreting fMRI signal.</p

Distinct neurochemical influences on fMRI response polarity in the striatum

The striatum, known as the input nucleus of the basal ganglia, is extensively studied for its diverse behavioral roles. However, the relationship between its neuronal and vascular activity, vital for interpreting functional magnetic resonance imaging (fMRI) signals, has not received comprehensive examination within the striatum. Here, we demonstrate that optogenetic stimulation of dorsal striatal neurons or their afferents from various cortical and subcortical regions induces negative striatal fMRI responses in rats, manifesting as vasoconstriction. These responses occur even with heightened striatal neuronal activity, confirmed by electrophysiology and fiber photometry. In parallel, midbrain dopaminergic neuron optogenetic modulation, coupled with electrochemical measurements, establishes a link between striatal vasodilation and dopamine release. Intriguingly, in vivo intra-striatal pharmacological manipulations during optogenetic stimulation highlight a critical role of opioidergic signaling in generating striatal vasoconstriction. This observation is substantiated by detecting striatal vasoconstriction in brain slices after synthetic opioid application. In humans, manipulations aimed at increasing striatal neuronal activity likewise elicit negative striatal fMRI responses. Our results emphasize the necessity of considering vasoactive neurotransmission alongside neuronal activity when interpreting fMRI signal.</p