Cardiac Physiology

Research Impact/Research Interest

Cardiac muscle plays a crucial role in generating pressure in the cardiac chamber and controlling the amount of blood ejected from the heart.  As the highest cause of mortality rate in the whole world population, search for prevention and treatment of heart disease is the most excitement and dedication.  Thus, the going on research project in our laboratory has been mainly focused on understanding the role of sex hormones on physiological function as well as pathological intervention of the heart.

Scope of Research

Female Sex Hormones & Cardiac Function
          A lower heart disease incidence in young women than that of age-matched men indicates the influence of gender difference in cardiac function.  Disappearance of this cardiac advantage after menopause thus suggests the cardio-protective effect of female sex hormones.  The evidence has led us to a long series of experimental investigations using ovariectomized rat as the model of study to demonstrate many effects of female sex hormone deprivation including:

1. A decreased maximum cardiac myofilament Ca2+ ATPase activity.

2. An increased cardiac myofilament Ca2+ sensitivity.

3. A shift of myosin heavy chain toward more b-isoform.

4. Upregulation of cardiac b1-adrenergic receptors.

5. A decreased amplitude of intracellular Ca2+ transients with a prolonged Ca2+ decay time.

6. A decreased peak shortening with prolonged relaxation of the cardiac myocyte.

7. Decreases in maximum SR Ca2+ uptake and maximum SERCA activity.

8. An increase in the SERCA Ca2+ sensitivity.

9. Downregulation of SERCA2a protein.

10. A decreased phosphorylation level of phospholamban at theronine-17 site.

11. An increased cardiac NHE1 activity.

12. Deterioration of cardiac mitochondrial structure and function.

13. Alteration of cardiac mast cell number and activity.

Female Sex Hormones & Heart Disease Challenge
          Cardio-protective roles of female sex hormones have been elucidated by challenging with pathological insults like diabetes or angiotensin II-induced hypertension. Our previous results and going on experiments show interactive actions of female sex hormones and diabetes or angiotensin II on cardiac functions in the following aspect:

1. No synergistic interaction of ovarian sex hormone deficiency and diabetes on maximum cardiac myofilament Ca2+ ATPase activity.

2. Cardiac myofilament Ca2+ hypersensitivity after ovarian sex hormones deprivation still existes under diabetic complication.

3. The shift in myosin heavy chain isoforms in ovariectomized rat heart is not the only mechanism underlying the reduction of maximum cardiac myofilament Ca2+ ATPase activity.

4. The presence of female sex hormones increases myocardial stiffness and cardiac collagen content in diabetic rat.

5. Female sex hormones prevent the change in length-dependent myofilament Ca2+ sensitivity induced by diabetes.

6. Female sex hormones have no effect on myocardial stiffness under chronic angiotensin-II induction.

Male Sex Hormones & Cardiac Function
          Despite an indication of gender difference in cardiac function from the lower heart disease incidence in young women than that of age-matched men, a higher prevalence of cardiac dysfunction is still observed in men who have low plasma testosterone level.  On the other hand, the athlete who receives over dose of anabolic steroid such as testosterone for a long period of time would develop pathological hypertrophy of the heart with a potential of cardiac sudden death.  It is therefore interesting to investigate the regulatory role of male sex hormones on cardiac function in both aspects of hormone lacking and overdose.  We have demonstrated preliminary results concerning effects of male sex hormone deprivation using castrated rat model to include

1. A decreased maximum cardiac myofilament Ca2+ ATPase activity.

2. No change in cardiac myofilament Ca2+ sensitivity.

3. A shift of myosin heavy chain toward more b-isoform.

4. A decreased maximum SERCA activity with downregulation of SERCA2a protein.

5. A Ca2+ hypersensitivity of SERCA.

6. Potentiation of ROS production without alteration of mitochondrial structure and ATP production.

The pharmacological effect of male sex hormones on cardiac function has also been investigated.  Results from both time-and dose-dependent studies reveals that high dose of testosterone induces:

1. Cardiac hypertrophy with neither time- nor dose-dependence.

2. A decrease in maximum force contraction in a time dependent manner.

3. An increase in myocardial stiffness without time- and dose-dependence.

4. Bi-phasic changes in SERCA activity and SERCA2a expression in a dose-dependent manner.

5. Neither change in NCX activity nor protein expression.

Female Sex Hormones & Exercise Training on Cardiac Function
         Though female sex hormones exert many beneficial outcomes to the heart, the use of hormone replacement therapy in postmenopausal women still gives rise to a risk of developing breast cancer.  We are then also interested in finding feasible alternatives to prevent cardiac dysfunction especially after menopausal period.  Our approach of introducing exercise training at moderate intensity to the ovariectomized rat clearly demonstrates a cardio-preventive outcome as expected.


1. Professor Dr. Jonggonnee Wattanapermpool

2. Associate Professor Dr. Tepmanas Bupha-Intr

3. Dr. Chutima Rattanasopa

Graduate Students

1. Miss Munthana  Wadthaisong

2. Miss Sukanya  Phungphong

3. Mr. Theerachat Kampaengsri

4. Mr. Rerknapat Jitmana

5. Mr. Thanwa Supimarot

Research Collaborations

- National

1. Assist. Prof. Anusak Kijtawornrat D.V.M., Ph.D.                                                      (Veterinary Biosciences, Chulalongkorn University)

2. Assist. Prof. Marisa Ponpuak (Department of Microbiology, Faculty of Science, Mahidol University)

3. Dr. Amornrat Naranuntarat Jensen (Department of Pathobiology, Faculty of Science, Mahidol University)

- International

1. Prof. Dr. Pieter de Tombe (Department of Physiology and Biophysics, University of Illinois) (Heart Science Centre, Imperial College London)

2. Assist. Prof. Dr. Jonathan Kirk (Loyola University Chicago Stritch School of Medicine)


Prof. Dr. Jonggonnee Wattanapermpool

ศ.ดร.จงกลณี วัฒนาเพิ่มพูล

Assoc. Prof. Dr. Tepmanas Bupha-Intr, D.V.M.

รศ.ดร.เทพมนัส บุปผาอินทร์

(Principal Investigator)


  • Munthana Wadthaisong
  • Theerachat Kampaengsri
  • Sukanya Phungphong
  • Thunwa Supimarot
  • Rerknapat Jitmana

Research Collaboration

- National