Tags

Type your tag names separated by a space and hit enter

Investigating the involvement of TRPV1 ion channels in remote hind limb preconditioning-induced cardioprotection in rats.
Naunyn Schmiedebergs Arch Pharmacol. 2017 Feb; 390(2):117-126.NS

Abstract

Remote ischemic preconditioning (RIPC) treatment strategy is a breakthrough in the field of cardiovascular pharmacology as it has the potential to attenuate myocardial ischemia-reperfusion injury. However, the underlying intracellular pathways have not been widely explored. The present study intends to explore the possible role of TRPV1 channels in mediating remote hind limb preconditioning-induced cardioprotection. Remote hind limb preconditioning stimulus (4 cycles in succession) was delivered by tying the blood pressure cuff at the inguinal level of the rat. The Langendorff system was used to perfuse the isolated heart and afterward was subjected to 30 min of global ischemia and 120 min of reperfusion. Sustained ischemia and, thereafter, reperfusion led to cardiac injury that was assessed in terms of infarct size, lactate dehydrogenase (LDH) release, creatine kinase (CK) release, left ventricular end diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), +dp/dtmax, -dp/dtmin, heart rate, rate pressure product, and coronary flow rate. The pharmacological modulators employed included capsaicin as TRPV1 agonist and capsazepine as TRPV1 antagonist. Remote hind limb preconditioning stimulus and capsaicin preconditioning (5 and 10 mg/kg) led to significant reduction in infarct size, LVEDP, LDH release, CK release, and significant improvement in LVDP, +dp/dtmax, -dp/dtmin, heart rate, rate pressure product, and coronary flow rate. However, remote hind limb preconditioning-induced cardioprotective effects were considerably abolished in the presence of capsazepine (2.5 and 5 mg/kg). This indicates that remote hind limb preconditioning stimulus possibly activates TRPV1 channels to produce cardioprotective effects.

Authors+Show Affiliations

Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, 147002, India.Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, 147002, India. amteshwarjaggi@yahoo.co.in.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27752734

Citation

Randhawa, Puneet Kaur, and Amteshwar Singh Jaggi. "Investigating the Involvement of TRPV1 Ion Channels in Remote Hind Limb Preconditioning-induced Cardioprotection in Rats." Naunyn-Schmiedeberg's Archives of Pharmacology, vol. 390, no. 2, 2017, pp. 117-126.
Randhawa PK, Jaggi AS. Investigating the involvement of TRPV1 ion channels in remote hind limb preconditioning-induced cardioprotection in rats. Naunyn Schmiedebergs Arch Pharmacol. 2017;390(2):117-126.
Randhawa, P. K., & Jaggi, A. S. (2017). Investigating the involvement of TRPV1 ion channels in remote hind limb preconditioning-induced cardioprotection in rats. Naunyn-Schmiedeberg's Archives of Pharmacology, 390(2), 117-126. https://doi.org/10.1007/s00210-016-1311-x
Randhawa PK, Jaggi AS. Investigating the Involvement of TRPV1 Ion Channels in Remote Hind Limb Preconditioning-induced Cardioprotection in Rats. Naunyn Schmiedebergs Arch Pharmacol. 2017;390(2):117-126. PubMed PMID: 27752734.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Investigating the involvement of TRPV1 ion channels in remote hind limb preconditioning-induced cardioprotection in rats. AU - Randhawa,Puneet Kaur, AU - Jaggi,Amteshwar Singh, Y1 - 2016/10/17/ PY - 2016/08/08/received PY - 2016/10/09/accepted PY - 2016/10/19/pubmed PY - 2017/2/22/medline PY - 2016/10/19/entrez KW - Cardioprotection KW - Ischemia KW - Remote preconditioning KW - TRPV1 channels SP - 117 EP - 126 JF - Naunyn-Schmiedeberg's archives of pharmacology JO - Naunyn Schmiedebergs Arch Pharmacol VL - 390 IS - 2 N2 - Remote ischemic preconditioning (RIPC) treatment strategy is a breakthrough in the field of cardiovascular pharmacology as it has the potential to attenuate myocardial ischemia-reperfusion injury. However, the underlying intracellular pathways have not been widely explored. The present study intends to explore the possible role of TRPV1 channels in mediating remote hind limb preconditioning-induced cardioprotection. Remote hind limb preconditioning stimulus (4 cycles in succession) was delivered by tying the blood pressure cuff at the inguinal level of the rat. The Langendorff system was used to perfuse the isolated heart and afterward was subjected to 30 min of global ischemia and 120 min of reperfusion. Sustained ischemia and, thereafter, reperfusion led to cardiac injury that was assessed in terms of infarct size, lactate dehydrogenase (LDH) release, creatine kinase (CK) release, left ventricular end diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), +dp/dtmax, -dp/dtmin, heart rate, rate pressure product, and coronary flow rate. The pharmacological modulators employed included capsaicin as TRPV1 agonist and capsazepine as TRPV1 antagonist. Remote hind limb preconditioning stimulus and capsaicin preconditioning (5 and 10 mg/kg) led to significant reduction in infarct size, LVEDP, LDH release, CK release, and significant improvement in LVDP, +dp/dtmax, -dp/dtmin, heart rate, rate pressure product, and coronary flow rate. However, remote hind limb preconditioning-induced cardioprotective effects were considerably abolished in the presence of capsazepine (2.5 and 5 mg/kg). This indicates that remote hind limb preconditioning stimulus possibly activates TRPV1 channels to produce cardioprotective effects. SN - 1432-1912 UR - https://www.unboundmedicine.com/medline/citation/27752734/Investigating_the_involvement_of_TRPV1_ion_channels_in_remote_hind_limb_preconditioning_induced_cardioprotection_in_rats_ L2 - https://dx.doi.org/10.1007/s00210-016-1311-x DB - PRIME DP - Unbound Medicine ER -