1. MECHANISMS OF INTERCELLULAR COMMUNICATION

2. INTERNET RESOURCES http://www.vivo.colostate.edu/hbooks/path phys/endocrine/index.htmlhttp://www.vivo.colostate.edu/hbooks/path phys/endocrine/index.html http://www.uri.edu/pharmacy/animation/hu angAnim.htmhttp://www.uri.edu/pharmacy/animation/hu angAnim.htm http://www.infochembio.ethz.ch/links/en/bi ochem_hormone.htmlhttp://www.infochembio.ethz.ch/links/en/bi ochem_hormone.html http://www.scientia.org/cadonline/Biology/ endocrine/action.ASPhttp://www.scientia.org/cadonline/Biology/ endocrine/action.ASP

3. TYPES OF INTERCELLULAR COMMUNICATION DIRECT COMMUNICATION SYNAPTIC COMMUNICATION AUTOCRINE COMMUNICATION PARACRINE COMMUNICATION ENDOCRINE COMMUNICATION –http://www.wisc- online.com/objects/index_tj.asp?objid=AP137 04

4. DIRECT COMMUNICATION GAP JUNCTIONS CYTOPLASM TO CYTOPLASM IONS SMALL MOLECULES IN SOLUTION LIPID SOLUBLE MOLECULES LIMITED TO ADJACENT CELLS

5. SYNAPTIC COMMUNICATION NEUROTRANSMITTERS SYNAPTIC CLEFTS LIMITED TO SPECIFIC AREAS

6. LOCAL CHEMICAL MESSENGERS AUTOCRINE PARACRINE

7. ENDOCRINE COMMUNICATION TARGET CELLS THROUGHOUT BODY HORMONES CARRIED IN CIRCULATORY SYSTEM

8. DIFFERENCES BETWEEN NERVOUS AND ENDOCRINE SYSTEMS NERVOUS ENDOCRINE FREQUENCY- MODULATED SIGNALS FASTER ACTING SHORT DURATION GENERALLY LESS DISTRIBUTED AMPLITUDE- MODULATED SIGNALS LONGER ACTING LONGER DURATION GENERALLY MORE WIDELY DISTRIBUTED

9. RELATIONSHIP BETWEEN ENDOCRINE AND NERVOUS CANNOT BE SEPARATED ANATOMICALLY OR FUNCTIONALLY NEURONS INNERVATE ENDOCRINE GLANDS SOME NEURONS SECRETE NEUROHORMONES INTO BLOOD SOME HORMONES AFFECT NERVOUS SYSTEM

10. TYPES OF MESSENGERS AMINO ACID DERIVATIVES PEPTIDE HORMONES LIPID DERIVATIVES

11. AMINO ACID DERIVATIVES SIMILAR TO AMINO ACIDS BIOGENIC AMINES CATECHOLAMINES –EPINEPHRINE –NOREPINEPHRINE –DOPAMINE THYROID HORMONE MELATONIN

12. PEPTIDE HORMONES CHAINS OF AMINO ACIDS SHORT PEPTIDE CHAINS

13. LIPID DERIVATIVES STERIOD HORMONES EICANOSOIDS

14. STEROIDS LIPIDS SIMILAR TO CHOLESTEROL ANDROGENS PROGESTINS ESTROGENS CORTICOSTEROIDS CALCITROL

15. EICOSANOIDS LIPID DERIVATIVES OF ARACHIDONIC ACID LEUKOTRIENES PROSTAGLANDINS THROMBOXANES PROSTACYCLINES

16. HORMONE REGULATION HORMONE SECRETION INCREASES AND DECREASES USUALLY CONTROLLED BY NEGATIVE FEEDBACK

17. MECHANISMS OF CONTROL ACTION OF SUBSTANCES OTHER THAN HORMONES NEURAL CONTROL OF ENDOCRINE GLAND ACTIVITY OF ONE ENDOCRINE GLAND CONTROLLED BY HORMONES FROM ANOTHER

18. ACTION OF SUBSTANCES OTHER THAN HORMONES CONCENTRATION OF GLUCOSE IN BLOOD AFFECTS INSULIN AND GLUCAGON SECRETION CONCENTRATION OF CALCIUM IN BLOOD AFFECTS CALCITONIN AND PARATHYROID HORMONE SECRETION

19. CONTROL OF INSULIN SECRETION BY BLOOD GLUCOSE LEVELS ELEVATED BLOOD LEVELS OF GLUCOSE STIMULATE INSULIN SECRETION INSULIN ACTS ON TARGET TISSUES TO INCREASE UPTAKE AND USE OF GLUCOSE DECLINING BLOOD LEVELS OF GLUCOSE LEAD TO A DECREASE IN INSULIN PRODUCTION

20. CONTROL OF ADRENAL MEDULLARY SECRETIONS BY NEURAL MECHANISMS STRESS ACTIVATES SYMPATHETIC DIVISION OF THE ANS SYMPATHETIC NEURONS STIMULATE RELEASE OF EPINEPHRINE AND NOREPINEPHRINE FROM ADRENAL MEDULLA WHEN STRESS IS REMOVED EPINEPHRINE AND NOREPINEPHRINE LEVELS DECLINE

21. HORMONES CAN STIMULATE OR INHIBIT SECRETON OF OTHER HORMONES

22. CONTROL OF THYROID STIMULATING HORMONE BY THYROID RELEASING HORMONE TRH IS RELEASED BY NEURONS IN HYPOTHALAMUS STIMULATES RELEASE OF TSH FROM ANTERIOR PITUITARY TSH STIMULATES SECRETION OF THRYOID HORMONE FROM THYROID CONTROLLED BY NEGATIVE FEEDBACK

23. HORMONES MAY BE CONTROLLED BY ONE OR MORE OF THESE MECHANISMS

24. POSITIVE FEEDBACK MECHANISMS ARE USED NEGATIVE FEEDBACK MECHANISMS LIMIT PROCESSES

25. MENSTRUAL CYCLE BEFORE OVULATION POSITIVE FEED BACK

26. MENSTRUAL CYCLE AFTER OVULATION NEGATIVE FEED BACK MECHANISMS

27. TRANSPORTATION OF HORMONES FREE STATE BOUND TO PLASMA PROTEINS THYROID BINDING GLOBULIN TRANSTHYRETIN ALBUMIN TRANSCORTIN

28. HORMONES TRANSPORTED IN BOUND FORM EQUILIBRIUM EXISTS BETWEEN FREE AND BOUND FORM PREVENTS LARGE INCREASES OR DECREASES IN HORMONE LEVELS

29. EXAMPLES THRYOID HORMONES ARE CARRIED BY THYROID BINDING GLOBULIN AND ALBUMIN PROGESTERONE IS CARRIED BY TRANSCORTIN AND ALBUMIN

30. DISTRIBUTION OF HORMONES WIDELY DISTRIBUTED DIFFUSE INTO INTERSTITIAL FLUIDS RATES OF DIFFUSION VARY

31. METABOLISM AND ELIMINATION OF HORMONES LIMITS TO LENGTH OF TIME HORMONES ARE ACTIVE ALLOWS MORE PRECISE REGULATION

32. HALF LIFE TIME IT TAKES FOR HALF A DOSE OF A SUBSTANCE TO BE ELIMINATED FROM CIRCULATORY SYSTEM

33. SHORT HALF LIFE HORMONES HORMONES WITH SHORT HALF LIVES INCREASE AND DECREASE RAPIDLY IN PLASMA WATER SOLUBLE HORMONES

34. LONG LIFE HORMONES HORMONES WITH LONG HALF LIVES HAVE RELATIVE STABLE LEVELS IN PLASMA STEROID HORMONES

35. FACTORS THAT INFLUENCE THE HALF LIFE OF HORMONES ELIMINATION –EXCRETION –METABOLISM –CONJUGATION –ACTIVE TRANSPORT CONSERVATION –PROTECTION FROM EXCRETION –PROTECTION FROM METABOLISM –PROTECTION BECAUSE OF HORMONE STRUCTURE

36. HORMONAL INTERACTIONS WITH TARGET CELLS HORMONES BIND TO TARGET CELL RECEPTORS ALTER RATE OF CELLULAR ACTIVITIES ACTIVATE OR INACTIVATE ENZYMES INCREASE OR DECREASE RATE OF SYNTHESIS OF MOLECULES IN CELLS CAUSES CHANGES CELL MEMBRANE PERMEABILITY

37. HORMONE RECEPTORS PROTEIN OR GLYCOPROTEIN EACH RECEPTOR HIGHLY SPECIFIC FOR ITS HORMONE A HORMONE MAY HAVE DIFFERENT RECEPTORS TARGET CELLS HAVE RECEPTORS- NONTARGET CELLS DO NOT

38. RECEPTORS AND DOWNREGULATION NUMBER OF RECEPTORS DECREASE AFTER EXPOSURE TO CERTAIN HORMONES RESPOND TO SHORT TERM INCREASES IN HORMONE CONCENTRATIONS

39. MECHANISMS OF DOWN REGULATION RECEPTOR SYNTHESIS DECREASES COMBINATION OF HORMONES AND RECEPTORS INCREASE RATE OF RECEPTOR MOLECULE DEGRADATION

40. RECEPTORS AND UP REGULATION SOME TISSUES EXHIBITG PERIODIC INCREASES IN SENSITIVITY TO CERTAIN HORMONES THE EXPOSURE OF A TISSUE TO ONE HORMONE INCREASES ITS SENSITIVITY TO ANOTHER

41. TYPES OF RECEPTORS MEMBRANE BOUND INTRACELLLULAR

42. MEMBRANE BOUND RECEPTORS WATER SOLUBLE HORMONES REVERSIBLE BINDING EQUILIBRIUM EXISTS

43. CHARACTERISTICS OF HOMONE RECEPTORS OF THE CELL MEMBRANE GENERALLY LARGE MOLECULES ALMOST ALWAYS HIGHLY SPECIFIC FOR SINGLE HORMONE INACTIVE WHEN HORMONE IS NOT BOUND TO IT

44. EFFECT OF HORMONAL BINDING TO RECEPTORS SELDOM DIRECTLY AFFECT INTRACELLULAR MACHINERY BINDING USUALLY ACTIVATES CELLULAR PROCESSES SOMETIMES BINDING INACTIVATES CELLULAR PROCESSES DIRECT OR INDIRECT EFFECTS

45. DIRECT EFFECTS CONFORMATIONAL CHANGE OF RECEPTOR MOLECULE CHANGES MEMBRANE PERMEABILITY ESPECIALLY SODIUM, CHLORIDE AND CALCIUM IONS ACETYLCHOLINE—a neurotransmitter SEROTONIN---a hormone and neurotransmitter GLYCINE—a neurotransmitter GABA---a neurotransmitter GROWTH HORMONE---a hormone

46. INDIRECT EFFECTS HORMONES THAT ACTIVATE G PROTEINS AND ALTER MEBRANE CHANNELS OR ACTIVATE INTRACELLULAR MEDIATORS HORMONES THAT ALTER ACTIVITY OF INTRACELLULAR ENZYMES TO CATALYZE SYNTHESIS OR PHOSPHORYLATION

47. HORMONES THAT ACTIVATE G PROTEINS OXYTOCIN VASOPRESSIN LUTEINIZING HORMONE FOLLICLE STIMULATING HORMONE PROLACTIN ATRIAL NATRIURETIC HORMONE THYROID STIMULATING HORMONE PARATHYROID HORMONE GLUCAGON EPINEPHRINE ADRENOCORTICOTROPI C HORMONE

48. EFFECTS OF HORMONE BINDING REGULATION OF MEMBRANE CHANNELS INCREASING OR DECREASING INTRACELLULAR MEDIATORS c GMP & c AMP

49. HOW G PROTEINS REGULATE THE SYNTHESIS OF INTRACELLULAR MEDIATORS G PROTEIN ALTERS ACTIVITY OF ENYZMES AT INNER SURFACE OF CELL MEMBRANE ADENYL CYCLASE & GUANYL CYCLASE INCREASES OR DECREASES c AMP OR c GMP LEVELS IN CELL

50. Cyclic AMP AS AN INTRACELLULAR MEDIATOR PROTEIN AND POLYPEPTIDE HORMONES CTH, TSH, LH, FSH, ADH, PTH, GLUCAGON, CATECHOLAMINES, SECRETIN AND HYPOTHALAMIC RELEASING HORMONES ACT BY cyclic ADENOSINE MONOPHOSPHATE MECHANISM

51. ADENOSINE MONOPHOSPHATE SECOND MESSENGER SYSTEM HORMONE IS FIRST MESSENGER BINDS TO RECEPTOR ON OUTER SURFACE OF CELL MEMBRANE RECEPTOR ASSOCIATED A G PROTEIN SOME EXCITATORY-SOME INHIBITORY

52. FUNCTION OF ADENYLATE CYCLASE CONVERTS ATP TO cyclic AMP

53. ACTIVITY OF cyclic AMP ACTIVATES OTHER ENZYMES USUALLY IN AN ENZYME CASCADE JUST A FEW cyclic AMP MOLECULES CAN HAVE POWERFUL EFFECT

54. PROTEIN KINASES ACTIVATED BY cyclic AMP USE PHOSPHATES AND ENERGY FROM ATP TO PHOSPHORYLATE ANOTHER ENZYME ACTIVATE OR INACTIVATE ENZYME OFTEN ACTIVATION OF ENZYME IS THE RATE LIMITING REACTION IN METABOLIC PATHWAY COMMON IN CELLS

55. EXCITATORY G PROTEINS ACTIVATES ADENYLATE CYCLASE

56. ACTION OF c AMP AND c GMP ACTIVATING cyclic AMP or cyclic GMP ACTIVATES PROTEIN KINASE/PHOSPHOKINASE

57. GLUCAGON EFFECTS ON LIVER CELLS ELEVATE cyclic AMP LEVELS ACTIVATE ENZYME SYSTEM PROMOTES BREAKDOWN OF GLYCOGEN INTO GLUCOSE

58. cyclic GUANOSINE MONOPHOSPHATE SECOND MESSENGER SYSTEM SOME CELLS USE INSTEAD OF cyclic AMP ATRIAL NATRIURETIC HORMONE NITRIC OXIDE

59. INTRACELLULAR MEDIATOR MOLECULES WILL HAVE DIFFERENT EFFECTS IN THE VARIOUS CELLS THAT USE THEM

60. G PROTEINS AND PHOSPOINOSITOL PHOSPHOLIPASE C ACTS ON PHOSPHOINOSITOL TO FORM DIACYLGLYCEROL & INOSITOL TRIPHOSPHATE INOSITOL TRIPHOSPHATE CAUSES RELEASE OF CALCIUM DIACYLGLYCEROL AND CALCIUM IONS ALTER ACTIVITY OF PROTEIN KINASES ALTER CALCIUM PERMEABILITY ALTER SYNTHESIS IN CELL

61. EFFECTS ON SMOOTH MUSCLE IN RESPONSE TO EPINEPHRINE INOSITOL TRIPHOSPHATE STIMULATES CALCIUM RELEASE FROM ENDPLASMIC RETICULUM AND/OR CELL MEMBRANE CALCIUM BINDS WITH CALMODULIN CALMODULIN BIND TO ENZYME THAT PHOSPHORYLATES MYOSIN MOLECULES TO STIMULATE CONTRACTION DIACYLGLYCEROL REGULATES ENZYMES THAT REGULATE SYNTHESIS OF PROSTAGLANDINS

62. HORMONE RECEPTORS THAT DIRECTLY SYNTHESIZE AN INTRACELLULAR MEDIATOR ATRIAL NATRIURETIC HORMONE BINDS WITH RECEPTOR GUANYLYL CYCLASE ACTIVATED PRODUCES cyclic GMP FROM GTP cyclic GMP CAUSES INCREASED EXCRETION OF SODIUM IONS INCREASED WATER VOLUME IN URINE

63. HORMONES THAT BIND TO RECEPTORS THAT PHOSPHORYLATE INTRACELLULAR HORMONES MEMBRANE BOUND RECEPTORS RECEPTOR ACTS AS PHOPHORYLASE ENCYME ATCHES PHOPHATE FROM ATPs TO RECPTOR AND INTRACELLULAR PROTEINS INSULIN GROWTH HORMONE,

64. CASCADE EFFECT FEW MEDIATOR MOLECULES ACTIVATE SEVERAL ENZYMES ACTIVATED ENZYMES ACTIVATE SEVERAL OTHER ENZYMES

65. INTRACELLULAR HORMONE RECEPTORS PROTEIN MOLECULES INSIDE CELL SOME FLOAT IN CYTOPLASM OTHERS IN NUCLEUS HORMONES BIND TO INTRACELLULAR RECEPTORS CALLED HORMONE RECEPTIVE ELEMENTS SEX STEROID MINERALOCORTICOIDS GLUCOCORTICOIDS THYROID HORMONE VITAMIN D

66. STEROID HORMONES DIFFUSE ACROSS CELL MEMBRANE BINDS TO DINA SEMENTS CALLED HORMONE RESPONSIVE ELEMENTS TRIGGERS ACTIVATION OR INACTIVATION OF SPECIFC GENES ALTERS TRANSCRIPTION RATE

67. ALDOSTERONE AFFECTS RENAL TUBULAR CELLS COMBINES WITH SPECIFIC RECEPTOR PROTEIN COMPLEX MOVES INTO NUCLEUS COMPLEX ACTIVATES SPECIFIC GENES m RNA IS FORMED AND DIFFUSES INTO CYTOPLASM TRANSLATION PRODUCES NEW PROTEINS PROTEINS PROMOTE SODIUM REABSORPTION INTO TUBULES AND SECRETION OF POTASSIUM INTO TUBULES TAKES FROM 45 MIN TO SEVERAL HOURS