rabbit polyclonal anti rat k ca 3 1  (Alomone Labs)

Journal: Frontiers in Cardiovascular Medicine

Article Title: Signaling and structures underpinning conducted vasodilation in human and porcine intramyocardial coronary arteries

doi: 10.3389/fcvm.2022.980628

Figure Lengend Snippet: K + channel-mediated vasodilation underlies conducted dilation of human and porcine RA-IMCAs. (A) Schematic of experimental setup with direction of flow of bradykinin (BK) indicated by carboxyfluorescein (CF). Micrographs showing an isolated, cannulated and pressurized human (B ) and porcine (C) artery. Focal application of BK (and CF, green) to the downstream end of the artery against the direction of superfusion flow caused local and conducted dilation in both human (D) and porcine (E) arteries. The corresponding time course of responses are shown in (F,G) , and , . A bolus of bradykinin was delivered at the point indicated by the arrow, and simultaneous inner diameter measured locally (0 μm) and up to 1,000 μm upstream, positions indicated by arrows in (D,E) . The same human artery used for K Ca 3.1 immunolabel in . Summary graphs show that compared to control ( n = 9, 14) neither L-NAME (100 μM, n = 3, 6) nor Ba 2+ (30 μM, n = 3, 3) affected local or conducted dilation, whereas depolarization to 45 mM KCl abolished conducted dilation ( n = 3, 6) in human (H) and porcine (I) arteries, respectively. Non-parametric mixed effects analysis with Sidak's multiple comparison test; * P < 0.05 vs. control.

Article Snippet: Primary antibodies were as follows: 1:100 rabbit polyclonal anti-rat K Ca 3.1 (aa 350–363; Alomone Laboratories, APC-064); 1:100 mouse monoclonal anti-human K Ca 3.1 (third extracellular loop; Alomone Laboratories, ALM-051); and 1:100 rabbit polyclonal anti-human K Ca 2.3 (aa 2–21, Alomone Laboratories, APC-025).

Techniques: Isolation, Immunolabeling

Journal: Frontiers in Cardiovascular Medicine

Article Title: Signaling and structures underpinning conducted vasodilation in human and porcine intramyocardial coronary arteries

doi: 10.3389/fcvm.2022.980628

Figure Lengend Snippet: K + channel expression and hyperpolarization to bradykinin in human and porcine IMCAs. Confocal micrographs of immunolabelling for K Ca 3.1 and K Ca 2.3 in isolated, cannulated and pressurized human (A) and porcine (B) RA-IMCAs with myogenic tone and full dilation to BK. Punctate and diffuse K Ca 3.1 label was evident in the ECs of human and porcine arteries, whereas K Ca 2.3 was less clear in human IMCAs, and highly expressed at EC borders of porcine IMCAs (yellow arrowheads). The elastin was dense in human arteries, with the internal elastic lamina (IEL) seen as longitudinal strings in the porcine arteries. Representative of at least 3 arteries for each label; asterisks indicate corresponding nuclei in upper and lower panels. The pink dashed line in the schematic represents the focal plane. (C) The schematic indicates a sharp microelectrode impaled into a SMC of a porcine RA-IMCA mounted for isometric tension recording. Under control conditions the thromboxane mimetic U46619 (0.6 μM) depolarized and contracted arteries, and BK (10 nM) caused hyperpolarization and relaxation (C) , summarized in (D) . (E) Addition of L-NAME depolarized and contracted porcine left ventricular (LV)-IMCAs. Under these conditions BK (0.1 nM to 100 nM) repolarized and relaxed the artery. Addition of 100 nM acetylcholine (ACh) depolarized and contracted the artery. The asterisk indicates when the electrode came out of the cell. The RMP and tension prior to the addition of L-NAME (100 μM) are indicated by dashed lines. Drugs were added to a static bath at the arrows. RMP, resting membrane potential.

Article Snippet: Primary antibodies were as follows: 1:100 rabbit polyclonal anti-rat K Ca 3.1 (aa 350–363; Alomone Laboratories, APC-064); 1:100 mouse monoclonal anti-human K Ca 3.1 (third extracellular loop; Alomone Laboratories, ALM-051); and 1:100 rabbit polyclonal anti-human K Ca 2.3 (aa 2–21, Alomone Laboratories, APC-025).

Techniques: Expressing, Isolation