Hypothesis / Introduction Prior studies have denoted gender differences in the expression and therapeutic benefits of hypertension treatment and clinical outcomes. This study documents for the first time gender differences in the expression of blood and urine angiotensin peptides in a normotensive Afro-Caribbean Barbadians (25 males; 26 females). Materials and Methods Participants provided clinical anthropometric measurements, 24 ambulatory blood pressure and urine collections, and a blood sample for measurements of angiotensin peptides. Results Plasma renin activity ranged between 0.00 – 3.00 ng/mL/h. Plasma and urinary Ang II were comparable in both genders while urinary Ang-(1–7) was greater in females (p<0.05). Urinary Ang-(1–7) and office systolic blood pressure correlated significantly in females only (p<0.01) while plasma Ang-(1–7) and Ang II correlated significantly in both genders (p>0.05). Conclusions A shift in the balance between Ang II and Ang-(1–7) and their respective pressor and depressor axes might be markers of the cardio-renal protective mechanisms that may be present in females of Afro-Caribbean descent.

The objective of this study was to determine whether plasmin could induce morphological changes in human glial cells via PAR1. Human glioblastoma A172 cells were cultured in the presence of plasmin or the PAR1 specific activating hexapeptide, SFLLRN. Cells were monitored by flow cytometry to detect proteolytic activation of PAR1 receptor. Morphological changes were recorded by photomicroscopy and apoptosis was measured by annexinV staining. Plasmin cleaved the PAR1 receptor on glial cells at 5 minutes (P = 0.02). After 30 minutes, cellular processes had begun to retract from the basal substratum and by 4 hours glial cells had become detached. Similar results were obtained by generating plasmin de novo from plasminogen. Morphological transformation was blocked by plasmin inhibitors aprotinin or epsilon-aminocaproic acid (P = 0.03). Cell viability was unimpaired during early morphological changes, but by 24 hours following plasmin treatment 22% of glial cells were apoptotic. PAR1 activating peptide SFLLRN (but not inactive isomer FSLLRN) promoted analogous glial cell detachment (P = 0.03), proving the role for PAR1 in this process. This study has identified a plasmin/PAR1 axis of glial cell activation, linked to changes in glial cell morophology. This adds to our understanding of pathophysiological disease mechanisms of plasmin and the plasminogen system in neuroinjury.

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The Afro-Caribbean sample has an inadequate daily potassium intake based on the observed intake and recommended values, with a high urinary excretion of the electrolyte compared to other values in the literature. This high potassium excretion could have been partly due to low plasma renin activity levels in the study participants. As a possible consequence, an increase in the nocturnal peripheral resistance is a likely cause for the diminished systolic dip. The lack of correlations between dietary potassium excretion and the blood pressure parameters does not allow any firm inference of the electrolyte's handling and its impact on cardiovascular health in the normotensive Afro-Caribbean participants. However, further research is needed to get a more accurate daily potassium intake value, and a more statistically robust sample to assess whether potassium handling and blood pressure would be affected by a change in potassium intake.

Aim: Urinary sodium excretion is used as an assessment tool for salt intake and salt handling. Even though cumbersome, the most reliable and readily used method in clinical and epidemiological studies is the 24-hour urine collection. This study investigates other appropriate means of predicting 24-hour urinary sodium excretion in a sample of Afro-Caribbeans in Barbados by assessing the correlation of actual and estimated urinary sodium excretion between a 24-hour urine collection sample, , and spot (AM and PM) urine collections. Method: A convenient sample of 30 healthy participants of Afro-Caribbean origin between the ages of 21 and 55 years was recruited for the study. The 24-hour urine samples and anthropometric data were collected as documented in the study's standard clinical procedure. A 24-hour urine sample was collected as two separate 12-hour AM and PM samples. In addition, two spot samples (AM and PM) were taken during each 12-hour sample collection period. Analysis of the urinary sodium and creatinine was done with a Roche/Hitachi Modular System (Roche Diagnostics, IN, USA). SPSS version 19 was used to analyse the data to make inferences. Results: Thirty Afro-Caribbean subjects participated in this study: 16 females and 14 males. The average age and body mass index (BMI) were 38 ± 17 years and 25.32 ± 5.98 kg/m 2 , respectively. The greatest correlation of the estimated 24-hour sodium excretion to the measured 24-hour sodium excretion was observed in the 12-hour PM sample (Pearson's correlation, r = 0.786, p < 0.001) followed by the 12-hour AM sample (Pearson's correlation, r = 0.774, p < 0.001). The PM spot sample showed a weaker, but still statistically significant correlation to the 24-hour timed sample (Pearson's correlation, r = 0.404, p < 0.045). The AM spot sample showed a very weak and insignificant correlation (Pearson's correlation, r = 0.05, p = 0.807) to the 24-hour timed sample. Similarly to the whole sample, the gender analysis demonstrated that estimated 24-hour sodium excretion in the female's 12-hour PM sample had the greatest correlation (r = 0.819, p < 0.001) to the measured 24hour sodium excretion, followed by the 12-hour AM (r = 0.793, p = 0.001) and the PM spot samples (r = 0.741, p = 0.02). The correlation between variables is weaker in males compared to the females. Conclusion: Overall, this study shows a clear correlation between the estimated 24-hour sodium excretion from the 12-hour timed PM sample and the measured 24-hour sodium excretion. Such findings support the thought of using other alternatives to determine sodium excretion, in view of replacing the cumbersome 24-hour urinary collection with a smaller timed sample. Nonetheless, a more robust and randomized population sample as well as a method to correct for high creatinine variability is required to further enhance the significance of the obtained results.