Journal: Biomolecules

Article Title: Trandolapril Attenuates Pro-Arrhythmic Downregulation of Cx43 and Cx40 in Atria of Volume Overloaded Hypertensive and Normotensive Rats

doi: 10.3390/biom15101457

Figure Lengend Snippet: Haematoxylin-eosin staining of the left (LA) and right atria (RA) of experimental rats. Abundant polymorphonuclear cells (asterisk) are present in the RA of normotensive HSD rats due to ACF-induced volume overload, which was attenuated by treatment with ACE inhibitors (ACEi) and angiotensin receptor blockers (ARB). Compared to HSD rats, the atria of hypertensive TGR exhibit a higher number of polymorphonuclear cells, with volume overload further enhancing their presence, particularly in the RA. This effect was attenuated by ACEi treatment. HSD—Hannover Sprague Dawley rats; TGR—Ren-2 transgenic rats; ACF—aortocaval fistula, surgical model of volume overload; ACEi—treatment with the angiotensin-converting enzyme inhibitor, trandolapril; ARB—treatment with an angiotensin II type 1 (AT 1 ) receptor blocker, losartan. Scale bar: 100 μm.

Article Snippet: Interestingly, Galectin-3 was significantly reduced in the right atria following treatment of volume-overloaded normotensive rats with either an ACEi or an ARB.

Techniques: Staining, Transgenic Assay

Journal: Biomolecules

Article Title: Trandolapril Attenuates Pro-Arrhythmic Downregulation of Cx43 and Cx40 in Atria of Volume Overloaded Hypertensive and Normotensive Rats

doi: 10.3390/biom15101457

Figure Lengend Snippet: Masson trichrom staining of interstitial and periarterial collagen fibers (blue color) in left (LA) and right atria (RA) of experimental rats. Cardiomyocytes are stained pink. An increase in collagen deposition due to ACF-induced volume overload is evident in the left (LA) and especially in the right atria (RA) of normotensive HSD rats, which was attenuated by treatment with ACE inhibitors (ACEi) or angiotensin receptor blockers (ARB). In hypertensive TGR rats, the LA showed baseline fibrosis that was not further exacerbated by volume overload, in contrast to the RA, which exhibited massive interstitial collagen accumulation. Treatment partially suppressed extracellular matrix alterations. HSD—Hannover Sprague Dawley rats; TGR—Ren-2 transgenic rats; ACF—aortocaval fistula, surgical model of volume overload; ACEi—treatment with the angiotensin-converting enzyme inhibitor, trandolapril; ARB—treatment with an angiotensin II type 1 (AT 1 ) receptor blocker, losartan. Scale bar: 100 μm.

Article Snippet: Interestingly, Galectin-3 was significantly reduced in the right atria following treatment of volume-overloaded normotensive rats with either an ACEi or an ARB.

Techniques: Staining, Transgenic Assay

Journal: Biomolecules

Article Title: Trandolapril Attenuates Pro-Arrhythmic Downregulation of Cx43 and Cx40 in Atria of Volume Overloaded Hypertensive and Normotensive Rats

doi: 10.3390/biom15101457

Figure Lengend Snippet: Alkaline phosphatase activity in the arterial capillary network (blue color) in the right (RA) and left atria (LA) of experimental rats. ACF-induced volume overload increased the density of arterial capillaries, particularly in the RA of normotensive HSD rats, along with elevated enzyme activity in the epicardium (white triangle), while the endocardium is highlighted with black triangles. These qualitative changes persisted despite treatment. In hypertensive TGR rats, the density of alkaline phosphatase-positive capillaries was higher in the RA compared to the LA and further enhanced in the LA following ACF. Treatment had no apparent effect. HSD—Hannover Sprague Dawley rats; TGR—Ren-2 transgenic rats; ACF—aortocaval fistula, surgical model of volume overload; ACEi—treatment with the angiotensin-converting enzyme inhibitor, trandolapril; ARB—treatment with an angiotensin II type 1 (AT 1 ) receptor blocker, losartan. Scale bar: 100 μm.

Article Snippet: Interestingly, Galectin-3 was significantly reduced in the right atria following treatment of volume-overloaded normotensive rats with either an ACEi or an ARB.

Techniques: Activity Assay, Transgenic Assay

Journal: Biomolecules

Article Title: Trandolapril Attenuates Pro-Arrhythmic Downregulation of Cx43 and Cx40 in Atria of Volume Overloaded Hypertensive and Normotensive Rats

doi: 10.3390/biom15101457

Figure Lengend Snippet: Dipeptidyl peptidase-4 (DPP4) activity (red color) in the venous capillary network of the left (LA) and right atria (RA) of experimental rats. Note the lower density and activity of DPP4 in the RA compared to the LA in both normotensive and hypertensive rats, regardless of intervention. White triangles indicate DPP4 activity in the epicardial region. HSD—Hannover Sprague Dawley rats; TGR—Ren-2 transgenic rats; ACF—aortocaval fistula, surgical model of volume overload; ACEi—treatment with the angiotensin-converting enzyme inhibitor, trandolapril; ARB—treatment with an angiotensin II type 1 (AT 1 ) receptor blocker, losartan. Scale bar: 100 μm.

Article Snippet: Interestingly, Galectin-3 was significantly reduced in the right atria following treatment of volume-overloaded normotensive rats with either an ACEi or an ARB.

Techniques: Activity Assay, Transgenic Assay

Journal: Biomolecules

Article Title: Trandolapril Attenuates Pro-Arrhythmic Downregulation of Cx43 and Cx40 in Atria of Volume Overloaded Hypertensive and Normotensive Rats

doi: 10.3390/biom15101457

Figure Lengend Snippet: Immunolabeling of connexin-43 (green color) revealed higher expression predominantly at the intercalated disks (double arrows) in the left (LA) and right atria (RA) of normotensive HSD rats. In contrast, lower myocardial expression of Cx43 and its mislocalization to the lateral membranes (single arrows) were observed in hypertensive TGR. ACF-induced volume overload reduced Cx43 expression in both atria of HSD rats, while the reduction was less pronounced in TGR. Moreover, volume overload increased the localization of Cx43 to the lateral membranes of cardiomyocytes in HSD rats, whereas lateral localization persisted in hypertensive TGR. Treatment with ACEi or ARB increased Cx43 levels and attenuated its mislocalization in both atria of HSD rats, and to a lesser extent in TGR. HSD—Hannover Sprague Dawley rats; TGR—Ren-2 transgenic rats; ACF—aortocaval fistula, surgical model of volume overload; ACEi—treatment with the angiotensin-converting enzyme inhibitor, trandolapril; ARB—treatment with an angiotensin II type 1 (AT 1 ) receptor blocker, losartan. The scale bar indicates 20 μm.

Article Snippet: Interestingly, Galectin-3 was significantly reduced in the right atria following treatment of volume-overloaded normotensive rats with either an ACEi or an ARB.

Techniques: Immunolabeling, Expressing, Transgenic Assay

Journal: Biomolecules

Article Title: Trandolapril Attenuates Pro-Arrhythmic Downregulation of Cx43 and Cx40 in Atria of Volume Overloaded Hypertensive and Normotensive Rats

doi: 10.3390/biom15101457

Figure Lengend Snippet: Protein levels of Cx43 ( A ) and Cx40 ( B ) normalized to GAPDH assessed by Western blot analysis. Hypertensive TGR rats exhibited lower levels of Cx43 and Cx40 in both the left and right atria compared to normotensive rats. A pronounced decrease in Cx43 and Cx40 protein levels was observed in both atria of normotensive HSD and hypertensive TGR rats due to volume overload. Treatment with an ACEi increased Cx43 and Cx40 levels ( p > 0.05) in both atria of volume-overloaded normotensive and hypertensive rats. In contrast, ARB treatment increased Cx43 but did not affect Cx40 levels in either atrium of volume-overloaded rats. HSD—Hannover Sprague Dawley rats; TGR—Ren-2 transgenic rats; ACF—aortocaval fistula, surgical model of volume overload; ACEi—treatment with the angiotensin-converting enzyme inhibitor, trandolapril; ARB—treatment with an angiotensin II type 1 (AT 1 ) receptor blocker, losartan. n = 10 per group. Data are presented as means ± SD; a p < 0.05 vs. HSD, b p < 0.05 vs. HSD ACF, c p < 0.05 vs. TGR, d p < 0.05 vs. TGR ACF. Western blot original images can be found in .

Article Snippet: Interestingly, Galectin-3 was significantly reduced in the right atria following treatment of volume-overloaded normotensive rats with either an ACEi or an ARB.

Techniques: Western Blot, Transgenic Assay

Journal: Biomolecules

Article Title: Trandolapril Attenuates Pro-Arrhythmic Downregulation of Cx43 and Cx40 in Atria of Volume Overloaded Hypertensive and Normotensive Rats

doi: 10.3390/biom15101457

Figure Lengend Snippet: Protein levels of PKCε ( A ) and PKCδ ( B ) normalized to GAPDH assessed by Western blot analysis. Compared to normotensive HSD rats, PKCε levels were lower in both the left and right atria of hypertensive TGR rats. ACF-induced volume overload significantly reduced PKCε protein levels only in the left atrium of normotensive HSD rats. Treatment with an ACEi increased PKCε levels in both atria of volume-overloaded normotensive HSD and hypertensive TGR. PKCδ protein levels were significantly increased in both the left and right atria of normotensive HSD and hypertensive TGR rats in response to volume overload. Treatment with an ACE inhibitor reduced PKCδ levels only in the left and right atria of volume-overloaded hypertensive TGR rats. HSD—Hannover Sprague Dawley rats; TGR—Ren-2 transgenic rats; ACF—aortocaval fistula, surgical model of volume overload; ACEi—treatment with the angiotensin-converting enzyme inhibitor, trandolapril; ARB—treatment with an angiotensin II type 1 (AT 1 ) receptor blocker, losartan. n = 10 per group. Data are presented as means ± SD; a p < 0.05 vs. HSD, b p < 0.05 vs. HSD ACF, c p < 0.05 vs. TGR, d p < 0.05 vs. TGR ACF. Western blot original images can be found in .

Article Snippet: Interestingly, Galectin-3 was significantly reduced in the right atria following treatment of volume-overloaded normotensive rats with either an ACEi or an ARB.

Techniques: Western Blot, Transgenic Assay

Journal: Biomolecules

Article Title: Trandolapril Attenuates Pro-Arrhythmic Downregulation of Cx43 and Cx40 in Atria of Volume Overloaded Hypertensive and Normotensive Rats

doi: 10.3390/biom15101457

Figure Lengend Snippet: Protein levels of MMP-2 ( A ), Galectin-3 ( B ), and ADAMTS ( C ) normalized to GAPDH assessed by Western blot analysis. MMP-2 protein levels were significantly reduced in both the left and right atria due to volume overload, but only in normotensive HSD rats. Treatment with an ACEi increased MMP-2 levels in the left atrium of volume-overloaded TGR rats. Galectin-3 protein levels were increased in the left atrium in response to volume overload, regardless of treatment. Interestingly, Galectin-3 levels were significantly reduced in the right atrium of volume-overloaded HSD rats treated with either an ACEi or an ARB. In contrast to the left atrium, Galectin-3 levels were significantly increased in the right atrium of volume-overloaded TGR rats. ADAMTS protein levels were not affected by volume overload in the left atrium, but were decreased in the right atrium of normotensive HSD rats. Notably, treatment with either an ACE inhibitor or an ARB increased ADAMTS protein levels in the left atrium of volume-overloaded TGR rats. Data are presented as means ± SD; a p < 0.05 vs. HSD, b p < 0.05 vs. HSD ACF, c p < 0.05 vs. TGR, d p < 0.05 vs. TGR ACF. Western blot original images can be found in .

Article Snippet: Interestingly, Galectin-3 was significantly reduced in the right atria following treatment of volume-overloaded normotensive rats with either an ACEi or an ARB.

Techniques: Western Blot

Journal: Journal of Pharmaceutical Policy and Practice

Article Title: Prescribing trends and patterns for antihypertensive agents in primary healthcare settings in Qatar: a retrospective observational study

doi: 10.1080/20523211.2025.2512183

Figure Lengend Snippet: Prescribing trends of antihypertensives among patients attending primary care setting in Qatar. ACEIs: angiotensin-converting enzyme inhibitors; CCBs: calcium channel blockers; ARBs: angiotensin receptor blockers.

Article Snippet: For instance, the PHCC guidelines recommend the use of ACEIs or ARBs as first-line therapy for diabetic patients with hypertension (Primary Health Care Corporation, ; National Institute for Health and Care Excellence, ).

Techniques: