Blood Pressure Regulation

1
Blood Pressure Regulation

• Controlled through Vasomotor center in
  brain-affected by feedback stimuli from several
  sources Rate Force of Heart Contractions-rising
  Q raises BP-SNS driven by NEpi Epi.
• Vasomotor tone of arteries-smooth muscle
  activation of smaller arterioles regulates
  peripheral resistance.Baroreceptors monitor
  changes in pressure, provide feedback for Degree
  of tone applied to arterioles

2
BP Control (cont)

• Activity of SNS to release NEpi on alpha receptor
  (vasoconstriction) and Epi on Beta receptor for
  vasodilation. Acts on a Set-Point Theory. 2)
  Kidney-regulates fluid volume in blood-retention
  of water raises volume Inc. BP
• SNS causes kidney releases hormone Renin
  -stimulates liver to use angiotensinogen to form
  Angiotensin I. Blood carries to lung,
  angiotensin II. Constrictor in arterioles.

3
Angiotensin II Effects

• Regulates reabsorption of sodium in kidney by
  stimulating aldosterone release from adrenal
  gland. Na retention controls fluid volume in
  kidney. Usually when BP rises Renin release
  decreases.
• Other factors-Atrial Naturetic Factor- causes
  kidneys to secrete more sodium, inhibits
  aldosterone renin production Nitric
  Oxide-endothelial cells-vasodilation

4
Causes of Hypertension

• Primary or essential Hypertension-no known cause-
  90-95-possibly..
• Genetics-overproduction of angiotensinogen in
  kidney-true gene defect. Excess water sodium
  retention-controversial
• Nitric Oxide abnormalities- inefficient release
  of NO-found inability to convert L-arginine to NO
  as a possible defect.
• Stress-High anxiety Inc. rates of Hi BP.

5
Secondary Hypertension

• Kidney disorder-chronic renal failure-excessive
  retention of salt water renovascular
  hypertensionexcessive amounts of renin released.
• Adrenal tumors-Aldosteronism hyper Epinephrine
  Norepi.
• Hyperthyroidism, excessive growth hormone, Inc.
  blood calcium due to parathyroid tumor.

6
Complications of Hypertension

• Stroke CHD-accelerate atherosclerotic
  process-leads to transient ischemic
  attacks-probably an exaggerated response to
  injury.
• Left Ventricular Hypertrophy-greater blood supply
  demand for LV, better chance for ischemia-leads
  to Congestive Heart Failure.
• Aneurysm-bulge in artery.
• Kidney Damage-narrow renal arteries.
• Syndrome X-caused by high Insulin.

7
Symptoms Signs

• Silent Killer majority of diagnoses occur with
  no prior knowledge-maybe headaches, blurred
  vision, drowsiness

8
Hypertension Medication

• B-blockers- blocks B receptor to slow down HR
  dec. contractility- dec. Q, dec. SNS, renin
  release, dec. work of heart. Angina Patients
  good- may lose ex. capacity due to low HR. Less
  training effect.
• Diuretics-increase renal excretion of salt
  water-prevent Na absorption at proximal distal
  tubule, Loop of Henle. Based on Na sensitive or
  kidney abnormalities. Loop, Thiazide,
  K-sparing.

9
Drugs Cont.

• Ca channel blockers-blocks slow inward flux of
  Ca, decrease smooth muscle contraction, lowers
  BP, maybe HR. Great choice for active
  people,coronary artery spasms. Also
  antiarhythmic.
• Nitrates- Nitroglycerin-venodilation decreases
  preload (LVV), some arterial dilation, may raise
  HR but less heart work. Prevents angina pectoris.

10
Peripheral Vasodilators

• Nonadrenergic vasodilators-direct relaxation of
  vascular smooth muscle. Use with B-blockade to
  dec. HR, and maybe diuretic for fluid retention.
• ACE-inhibitors-block formation of angiotensin II,
  vasoconstrictor aldosterone secretion).
• Peripheral Alpha-adrenergic antagonists-inhibit
  Epi or NE release,, deplete stores in nerve
  endings.

11
Finally, the end

• Alpha-blockade-interfere with nerve impulses
  which cause vasoconstriction.
• Central alpha-agonists-interfere with nerve
  impulses in brain-suppress sympathetic outflow-.
• Angiotensin II receptor blockade- Inhibits
  effects of Ang. II (vasoconstriction fluid
  retention.)

12
Exercise Training Hypertension

• Exercise evidence- does it reallly lower BP?? And
  does it reduce Hi BP incidence??
• 1) UPenn graduates- Real active alums had 1/3
  less Hi BP than active, and 40 less than
  Inactive.
• 2) Dallas, Tx, Lowfit group had 52 greater
  incidence of HI BP over 4 yrs.
• Typical exercise results- 11/9 mmHg drop for
  males 10/10 mmHg for females.

13
Potential Mechanisms

• Decrease in cardiac output and/or total
  peripheral resistance??? Both dictions have been
  found-Inconclusive to-date.
• Adrenergic Mechanisms-less NE release likely
  from peripheral tissues (muscle, skin lung).
• Neural Baroreflex-baroreflex attenuated (less
  responsive)-inhibiitory effect of cardiac
  afferents.

14
More Possibilities

• Metabolic mechanisms-Obesity leads to insulin
  resistance, and inc. NE levels. Good results in
  exercise causing wt. loss, dec. Insulin BP.
• Electrolyte Renal-Salt? I dont know? Usually
  low Ca K are markers for Hi BP. Goood
  results with Dialysis patients.
• Summary from ACSM Article??

15
Physical Activity, Physical Fitness Hypertension

• Role of exercise intensity-40-70 VO2max might
  lower BP more effectively than higher
  intensities.
• Most of decrease is in first 3 months. Yet
  benefit only lasts if exercise is continued.
• Least likely to benefit?-hypertensives with
  exaggerated exercise BP response to maximal
  exercise.

16
Death Rates, Fitness Hypertension

• Harvard Alumni, UPenn Alums experience up to a
  37 lower age-adjusted all-cause death rate than
  sedentary hypertensive alums. Cooper Clinic Fit
  Hypertensives had same all-cause mortality as
  normotensive sedentary subjects.
• Weight Loss, dec. Na intake, and biofeedback
  might produc similar benefits.

17
Activity BP Medication

• B-blockers may not be best choice save for
  subjects with real exaggerated rise in Systolic
  BP.
• ACE-inhibitors,Ca channel blockers alpha
  blockade are most likely first choice.
• Which drugs might also cancel other beneficial
  effects of exercise? Such as lowering HDL-C, Inc.
  TRIG or CHOL.

18
Even More Mechanisms

• Exercise may increase levels of circulating
  vasodilator substances-endorphins, and perhaps
  prostaglandins, adenosine, kinins, dopamine,
  atrial naturetic factor.
• Renal dysfunction-2ndary HBP reduce BP even
  further than primary-sign of renal/hormonal
  alteration.

19
Gender, Hypertension Exercise Hemodynamics

• 90 subjects, 4010 yrs tested at rest, at 50
  Watts cycle exercise, and at peak workload
  reached.
• SBP, DBP, LV-filling Press.,Q,HR,SV, TPR,VO2.
• Are any anticipated diff. due to body size?
• Adjust for HT. Wt. ANCOVA.

20
Resting Data
21
50 Watt Exercise
22
Peak Exercise Results
23
Major Findings

• Lower SV due primarily to smaller frame, yet
  persisted after adjustment for size.
• Mechanism not yet known? But leads to lower Q and
  VO2max at peak exercise.
• Arteriolar dilation in working muscles with
  exercise appears similar with gender since TPR
  was similar. Good for BP modelling with females.